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Lectures on Diseases of the Nervous System. 

SECOND SERIES. 



SUBJECTIVE SENSATIONS 

OF 

SIGHT AND SOUND, 

abiotrophy, 

and other lectures. 



BY 

SIR WILLIAM R. COWERS, M.D., F.R.C.P., F.R.S. 

HON. FELLOW R. COLL. PHYS. IRELAND; MEMBER OF THE SOC. 

MEDICINS RUSSSES OF ST. PETERSBURG AND OF THE 

ROYAL SOC. OF SCIENCE OF UPSALA, ETC. 



PHILADELPHIA : 

P. BLAKISTON'S SON & CO. 

IOI2 WALNUT STREET. 
1904. 



LIBRARY of CONGRESS 
Tw« C«pies Received 

JAN 29 1904 

Copyright Entry 

CLASS CL Ac. No. 

' COPY S \ 




/a 



Copyright, 1903, by P. Blakiston's Son & Co. 



WIM. F. FELL COMPANY, 

PRINTERS, 
PHILADELPHIA, U. S. A. 



PREFACE. 



The following Lectures, which have appeared in print at 
various times, have been carefully revised. The first lec-- 
ture has been throughout rewritten, and its substance re- 
arranged, in the light of later experience, which has not, 
however, modified its chief conclusions. These can only 
be extended by the collection of many other facts observed 
with care and recorded with precision. To promote such 
observations is one object of its republication. The second 
has also been carefully revised, and will likewise, I hope, 
promote more systematic study of a symptom which is apt 
to be passed over as too common to merit attention. Of 
the other lectures I need only say that the last, "On the 
Use of Drugs," although given some years ago, seems to 
need no change in consequence of fresh knowledge. There 
is indeed a prospect that our ultimate conceptions may be 
thrown into crucible, and recast by the influence of ardent 
thought, through the discoveries regarding radio-activity, 
and the possible nature of the elementary constituents of 
matter. But we must remember that these do not alter 
the coarser facts we were previously able to perceive. All 
that has been demonstrated regarding atoms and molecules, 
chemical affinities, and chemical compounds and com- 
binations, and the relation of these to energy, latent or 
released, remains true, whatever may be discerned of the 
ultimate nature of the processes. 

W. R. G. 



CONTENTS 



PAGE 

I. Subjective Visual Sensations, 9 

II. Subjective Sensations of Sound, 57 

III, Abiotrophy; Diseases from Defect of Life, 96 

IV. Myopathy and a Distal Form, ^ 121 

V. Metallic Poisoning, 140 

VI. Syphilitic Diseases of the Nervous System,* 158 

VII. Inevitable Failure, 184 

VIII. Syringal Haemorrhage into the Spinal Cord,* 200 

IX. Myasthenia and Ophthalmoplegia, 221 

X. The Use of Drugs, _* 236 



vu 



SUBJECTIVE SENSATIONS OF SIGHT 
AND OF SOUND 



OTHER LECTURES. 

LECTURE I. 

SUBJECTIVE VISUAL SENSATIONS. 

BEING 

THE BOWMAN LECTURE, 

Delivered to the Ophthalmological Society of London, on Friday, June 14th, i8gs. 



[The substance of this lecture has been rearranged, and it has been 
rewritten throughout.] 

Mr. President and Gentlemen: — The name of Bowman is 
associated alike with physiology and ophthalmology. The 
subject I have chosen for this lecture, given in grateful 
honour of his memory, combines these tw^o subjects with 
which that memory is linked. Apart from the results he 
achieved, already 'dimmed by the mists which so quickly veil 
the past, his name brings before us a singular grace of char- 
acter, and strenuous pursuit of the highest standard of scien- 
tific work, a standard we may not hope to reach, and yet 
may do better than otherwise if we keep it clearly in our 
view. 

2 9 



10 VISUAL SENSATIONS. 

The subject I ask you to consider to-day is that of the 
visual sensations that occur without external cause, sensa- 
tions of subjective nature. They are not rare, yet definite 
facts regarding their features are few. This is not surprising. 
That which is subjective can only be ascertained through the 
consciousness of another. We have to depend on description 
to enable us to conceive it; very rarely is depiction possible. 
Each presentation can be given us only by means of memory; 
the memory of any sensation is imperfect, and especially so 
when the visual sensation coincides with mental confusion. 
Hence the opportunities to obtain trustworthy facts are rare, 
and when secured they should be utilised to the utmost. 

In two diseases subjective visual sensations occur with 
special frequency, migraine and epilepsy, and in each they 
are often constant and precise. To these I propose to limit 
what I have to say and suggest, both for present thought and 
for future observation. 



PHYSIOLOGICAL CONSIDERATIONS. 

These subjective sensations present one relation which 
transcends all others in importance. This is the apparent 
relation of the sensations to the functions of the cerebral 
centres in which we must assume that they arise, and through 
which we must also assume conscious vision of external 
objects is achieved. In 1885 I put forth the opinion, which 
has been confirmed by all that I have since been able to 
perceive, that, in addition to the half-^dsion centre in the 
occipital lobe, demonstrated by Munk, the indications ob- 
tained by Ferrier are correct, and that there exists a higher 
visual centre in the region of the angular convolution, a 
centre which immediately subserves the perception of visual 
impressions. Impulses seem to pass to this higher centre in 
each hemisphere from both half-vision centres in the occi- 



PHYSIOLOGICAL CONSIDERATIONS. ii 

pital lobes, in such a way that in each higher centre both 
fields of vision are represented, but that of the opposite eye 
in greater degree. The connexion between the two higher 
centres is very intimate, and their function differs from that 
of the lower in two ways. First, it seems to present the 
mysterious feature that, while partial disease of the lower 
centre causes partial local loss of the related half-field, which 
cannot be compensated, partial disease of the higher centre 
seems to lower the function of the whole, and there is some 
capacity for compensation by the other hemisphere, although 
far less than in the lower animals. This may be one reason 
why the pathological evidence of this centre in man is so 
scanty, and another cause may be found in the fact that the 
centre is in the region of the blood-supply of two different 
arteries, and so is seldom entirely destroyed. In the strange 
hemianaesthesia of hysteria we have evidence of arrested 
action of all the higher special sense centres in one hemi- 
sphere. In this association we never meet with the hemiano- 
pia that results from disease of the lower centre in the pos- 
terior part of the hemisphere. Instead, we have the " crossed 
amblyopia," as it is termed; peripheral vision is lost in both 
eyes, central vision persists in a small area in the opposite 
eye, and in a larger area in the eye of the same side. No 
trace is found of any relation to the half-fields. But hysteria 
is a by- word, and all facts, however definite, with w^hich the 
name can be connected, are disregarded by physiologists. 
Yet they are definite, and must depend on equally definite 
functional arrangements. Moreover, the same affection of 
vision occurs in organic disease. I have given an illustration 
of it,* as a lasting symptom, in a case in which it was caused, 
with hemiplegia, by a sudden lesion, probably haemorrhage, in 



* Manual of Diseases of the Nervous System, vol. ii, second edition, 
Fig. 83 (first edition, Fig. 81). 



12 VISUAL SENSATIONS. 

one hemisphere. A similar loss has been met with when the 
angular region was found diseased.* When hemianopia is 
caused by disease of the cerebral hemisphere there is some- 
times a like contraction of the remaining half-fields, greater 
in the eye of the opposite side.f These may seem meagre 
grounds for the assertion that here we have a higher visual 
centre, but they agree in a remarkable way with the experi- 
mental results obtained by Ferrier, and a large number of 
the facts of disease cannot otherwise be understood. A 
theory that explains is not necessarily true. But if a theory 
affords an explanation which can be obtained in no other 
way, and has other varied and quite independent evidence, 
it seems to me that we are justified in its assumption. I 
have to ask you to postulate these higher visual centres, for 
I can best describe the facts of subjective sensation, and 
suggest their significance, by placing them in front of this 
hypothesis. 

Note the necessary significance of "crossed amblyopia." 
With loss of the higher visual centre of the left hemisphere, 
we have, in the right eye, vision only in a small central region ; 
in the left eye, sight remains in a larger central region. In 
each eye there is peripheral loss. The significance of this is 
that the vision which remains is subserved by the right 
higher centre acting alone. This subserves a large central 
region on the opposite side, a small central region on the 
same side, but, without the co-operation of the opposite 
centre, it cannot subserve peripheral vision in either eye. In 
the central regions of the fields, vision can be subserved by 
either hemisphere alone; in the peripheral parts, by neither 
alone. It is as if the impulses from the periphery of each 
retina ultimately reached the higher centre of one side through 



* Ibid., Fig. 15 (first edition, Fig. 14). 
■\ Ibid., Fig. 82 (first edition, Fig. 80). 



PHYSIOLOGICAL CONSIDERATIONS. 13 

that of the opposite side, — as if those from the peripheral 
region of each half- vision centre in the occipital lobe passed 
to the opposite hemisphere indirectly, through the higher 
centre of the same side, and those from the central region 
passed directly from the half-vision centre to each higher 
centre. So that, for instance, the peripheral impressions, to 
reach the right higher centre, have to pass through the higher 
centre on the left side, and the loss of this involves peripheral 
blindness on both sides. Whether this is so, or whether some 
other form of co-operation takes place, the facts show that the 
functional relation of the hemispheres is extremely close. It 
will be remembered that through the optic tract pass the 
fibres from the same side of each retina, receiving impressions 
from the opposite half of the field of each eye, and also from 
the whole of the small central region of the macula lutea, 
subserving central vision around the fixing point. The con- 
duction by each tract is to the occipital region of each 
hemisphere, the half-vision centre. Each of these lower 
centres receives the impulses from the whole of the corre- 
sponding half of each retina, i. e. the impressions from the 
opposite half of each field, and also from the whole macular 
region, so that destruction of either causes hemianopia up to 
the middle line except around the fixing-point, leaving cen- 
tral vision unimpaired. But the intimate connection between 
the visual centres of the two hemispheres is showm by the fact 
that an acute lesion in one lower, half-vision centre, which 
causes enduring hemianopia, may also cause for a few days 
absolute loss of sight, complete loss in both eyes, which can 
only be explained by a process of irritative inhibition of the 
visual centre on the undamaged side. This is of great im- 
portance for our present subject as a proof of the close 
connection of this function on the two sides, even in relation 
to the lower half- vision centres. Even more intimate must 
be the functional blending of the two higher visual centres 



14 VISUAL SENSATIONS. 

that we are compelled to assume, although each seems capa- 
ble of passing into a state of functional inaction. 

Colour- Vision. 

Subjective visual spectra frequently present colours — red, 
blue, yellow and sometimes green. One fact regarding these 
colour-sensations is that they are often referred to the pe- 
ripheral parts of the fields of vision, and are as distinct there 
as in the central region, to which their fields are said to 
be restricted. Green is supposed to have a very small colour- 
field, having a radius less than half that of the field for white. 
But, as an illustration of the way in which the subjective sen- 
sation transcends altogether the alleged limits of the field, I 
may mention a case of epilepsy in which the aura of the fit 
was uniformly a sensation of a green colour over the lower 
half of the field of vision, from side to side, so that the patient 
spontaneously said it was "as if he were standing in a field 
of grass." Such a subjective sensation is incompatible with 
the small size of the field for green as commonly described. 
But if an observer stands in an expanse of grass he will 
perceive the colour almost to the edge of the field of vision, 
and he will do so even if he covers the central part of the 
field. It is the same in the case of the blue of the sky; the 
blue is perceived to the edge of the field. This corresponds 
with the subjective sensation, but differs from the common 
statements regarding the colour fields. This difference led 
me to examine afresh the facts of peripheral colour vision. 
The results, I need hardly say, are not new, but they are not 
sufficiently recognised to make it superfluous for me to men- 
tion them. They have been known for nearly twenty years, 
since Chodin * worked at peripheral colour vision in regard 

* Archiv. fur Ophthalmologic, Band xxiii ; see also Landolt, A Manual 
of the Examination of the Eyes ; and Swanzy, Diseases of the Eye, p. 19. 



COLOUR-VISION. 



15 



to saturation. They were described by Landolt, but they do 
not seem famihar, to judge from the statements commonly 
made. The field in which red can be seen is described 
as a central region the limit of which crosses the outer hori- 
zontal radius at 45°. This hmit is even spoken of as "the 
boundary of the field for 
red. " But this is only the 
area in which red can be 
perceived in an object one 
centimetre square. The 
same statement in regard 
to a still smaller region 
is made respecting green. 
But with a larger area of 
colour it is found that all 
the colour-fields increase in 
size and ultimately differ in 
extent very little from the 
field for white. On the 
temporal side red can be 
seen as such up to 90°. 

Let us first take the red 
field (Fig. i). It is easy to 
ascertain that this depends 
in extent simply on the size 
of the coloured object. If 
we take the outer hori- 
zontal radius — that is the 
horizontal radius of the 

field in the temporal half, the limit of the region in which 
the colour can be discerned in an area half a centimetre 
square is, I find, at 35°, and for a quarter-centimetre square 
at 25° and in one centimetre square at 45°, commonly figured 
as the limit of the field for red. In an area two centimetres 




I. — The fields for red and green 
in areas of i, 5, and 6 centi- 
meters in concentric dimensions, 
and two-thirds in radial dimen- 
sion. (The latter is not accur- 
ately indicated in the black areas 
which represent the degrees oc- 
cupied by the object.) 



i6 VISUAL SENSATIONS. 

square, red is seen at 60°, three centimetres square at 70°, 
four at 78°, five at about 82°, ^yhile in an area of six centi- 
metres square the colour is seen up to the extreme edge of 
the field for white. Upwards, downwards, and on the nasal 
side of the field, in which the range of vision is so much more 
limited, the areal limits are closer together, so that on the 
inner horizontal radius the three-centimetre limit is at 40°, 
and the six- centimetre area of red can be seen at 50° — that 
is, at the edge of the field for white. Every field is practi- 
cally concentric with the field for white. In the case of blue 
and yellow still smaller areas suffice to permit the colour to 
be seen up to the edge of the field for Avhite. Green alone 
seems to fall short of the edge of the white field by about 5°. 

Colour. — I have spoken of areas of two or more centi- 
metres square. But this is not accurate. At each distance 
from the centre at which the colour can be seen in an area 
of a certain dimension, the same in the radial and in the 
concentric direction, it can be seen equally well if the radial 
dimension is only two-thirds of the concentric dimension. 
For instance, on the outer horizontal radius, red can be seen 
when an area 3 cm. square has its inner edge on the 70° 
circle. The colour can be seen equally well if the area three 
centimetres in the concentric direction is only two centi- 
metres wide, i. e. in the radial dimension. 

The influence of area is more easy to ascertain than is 
that of illumination. It is, moreover, of far greater practical 
importance, on account of the difficulty of securing condi- 
tions of illumination sufficiently constant for comparison, and 
of obtaining colours in sufficient saturation. Of red objects 
easily obtained, only the petals of flowers will bear reflected 
sunlight. Pigments reflect so much white light that the 
colour is often invisible. 

I have spoken of the mysterious way in which peripheral 
vision seems, in the higher centres, to be dependent on mutual 



COLOUR-VISION. 17 

co-operation, that in neither eye can peripheral vision occur 
unless the centres of both hemispheres are active, while in 
the central region there is vision in both eyes when only the 
higher centre in one hemisphere is active. This peculiar 
mutual influence of the centres is exemplified further by the 
colour-fields. The field for every colour-area is larger if both 
eyes are open. This seems natural so far as concerns the part 
of the two fields which overlap. But it is true also of that 
temporal part of each field which does not overlap. Binocu- 
lar intensification extends into this part, and extends into it 
in the same degree as in the part where the fields are double. 
For instance, let us take 

the outer (temporal) hori- ^^1 ^ ^ ^ |i | || 1 

zontal radius of the right "^ 10 20 50 40 50 60 70 80 90 
field (Fig. 2). In the x^ | | | | | ■ ! » ■ I 
single field (i. e. with the 

• , I . Fig. 2. — The outer horizontal radius of 

right eye only open, A) the right field, with the position on it 

red is seen in one centi- ^^ the limit of the red field for i, 2, 

and 4 cm. sq. A, With the left eye 
metre square at 42°, but closed; B, with the left eye open. The 

;., +1,^ ^^,,v.i^ -c u /,• o asterisk is at the fijdng point and the 

m^ the double field (i. e. ^.^.^.^^^ ^^ ^^o distance. 

with both eyes open, b) 

it is seen at 60°, although the left field only extends as far 
as 56°. In a square of two centimetres, red is seen in the 
single field at 62°, in the double field at 72°, and in a 
square of four centimetres it is seen in the single at 80°, 
while in the double field it can be perceived almost up to 
the edge at 90°. The fact that in the part of the fields in 
which each is single [i. e. is not covered by the other field) 
there is increased sensitiveness when both eyes act, gives addi- 
tional emphasis to the strange fact that, in this region, loss 
of one higher visual centre causes peripheral blindness. It 
shows how complete is the blending of function in the two 
centres. In this outer periphery, vision is impossible unless 
both higher centres act, but where the rays of coloured light 



i8 VISUAL SENSATIONS. 

fall on one retina only, their effect is greater if the other 
eye is open. Further observations show that there is a re- 
markable extension of each areal colour-field * if a small 
white area is in the central region, and that this extension 
is almost the same when it is opposite the other eye only. 
That is, simple increased stimulation of the central part of 
either retina augments the sensitiveness of the periphery to 
colour, and augments it equally whether it is the same or the 
other eye which is thus stimulated. These facts need more 
investigation, but they are clearly of importance in connection 
with the perception of colour at the periphery of the field 
in subjective sensations. They show that sensitiveness to 
colour not only involves the centres which are related to the 
periphery, but can be augmented by the functional activity 
of other parts. We must recognise the facts, although we 
cannot understand the process. I have ventured to men- 
tion this collateral physiology partly because it is related 
to the special subject, and partly on account of its intrinsic 
interest, and its unfamiliarity. 

From these physiological considerations, I may pass to 
the features of morbid action, as they are met with in asso- 
ciation with migraine and with epilepsy. 

/. VISUAL SENSATIONS IN MIGRAINE. 

It is convenient to begin the detailed consideration of the 
spontaneous visual sensations with those of migraine because 
they belong to a lower class than do those of epilepsy. They 
may seem complex in character, but are comparatively simple 
in nature. The epileptic visual auras are extremely brief, 
lasting a few seconds, and are followed by loss of conscious- 

* The term areal colour-field is convenient as a designation for the 
field in which colour can be perceived if it occupies a given area. 



VISUAL SENSATIONS IN MIGRAINE. 19 

ness and convulsions. The migrainous sensation is de- 
liberate, occupying a quarter to half an hour, and is followed 
by a headache lasting for hours. In rare cases similar sensa- 
tions occur as an isolated symptom, no headache following 
them. 

Not only are the sensations long in duration, but they 
present peculiar forms. The elementary features are few, 
but they have special varieties and combinations. They are 
always "crude" in nature, in the sense that they are low 
in the scale of sensory perceptions. No visions of objects or 
faces ever occur. Yet the sensation, simple in character, is 
remarkable in form, the simple elements develop in the most 
complex combinations and give rise to spectra that are ex- 
tremely curious, and will one day, I doubt not, be most 
instructive. For this instruction, much observation and 
comparison of facts is necessary. All I can hope to do is 
to stimulate others to the minute observation through which 
alone it may be possible to discern the true significance of 
the phenomena. 

Our knowledge of these spectra is chiefly due to the 
careful description of his own sensations by Dr. Hubert 
Airy, which appeared in the ' ' Philosophical Transactions of 
the Royal Society" for 1868. The plates have been repro- 
duced in Dr. Liveing's admirable treatise on Megrim, and 
an account of the phenomena has been given by Dr. Latham 
in his book on the disease. I am very fortunate in being able 
to show you to-night a series of other drawings, unpublished, 
which Dr. Airy has made of his sensations, accompanied by 
notes taken at the time. Another series of drawings of great 
value has been kindly made for me from his own sensations 

by a distinguished water colour artist, Mr. B . The 

peculiarity of the t3^pe of sensation and the manifest care of 
the drawings render them very important. Besides other 
miscellaneous sources of information I must mention espe- 



20 VISUAL SENSATIONS. 

cially some curious facts recorded by a man named Beck, who 
when sixty years of age, came under my care as an out- 
patient at the National Hospital for the Paralysed and Epi- 
leptic, and remained so until his death about five years later. 
During those years he was subject to the frequent appearance 
of visual spectra, very like those of migraine, but never 
attended with headache. He was not an educated man, but 
was a mechanical engineer and mechanical draughtsman. 
He was possessed by the idea that these spectra were ob- 
jective things, and he delighted in depicting them in the 
fashion of an engineering draughtsman. The result was the 
curious little book which I show you, and hand to the 
Society for custody.* It contains a number of delineations 
of these appearances, mechanical in character to an almost 
absurd degree, yet executed with precision in some features. 
They are accompanied by quaint descriptions, in which some 
degree of aphasia can be discerned. 



SPECIAL FEATURES OF MIGRAINOUS SPECTRA. 

The spectra of migraine present, as their most frequent 
feature, the zigzag or angled character, which is called the 
'' fortification spectrum" in its well-known curved character. 
It seems to be due to some opposing forces in the process, 
by which the discharge in a straight line cannot proceed 
beyond a short distance and is then compelled to give place 
to one at right angles to it. But we shall be able to con- 
sider its nature better in connection with its features. 

The visual discharge of migraine usually presents an 
association with a process of inhibition of function. The 
bright appearance is combined with an area in which vision 



* This book and Dr. Airy's valuable drawings are in the library of the 
Ophthalmological Society. 



SPECIAL FEATURES OF MIGRAINOUS SPECTRA. 21 

is dimmed or lost, but the relation of the two elements 
varies and is of great interest. Moreover, the loss of sight 
may seem to be simple, or may be attended itself by a subdued 
process of discharge, so that the area in which there is loss 
may present a dim luminosity, as if occupied by minute 
particles of luminous sand in constant molecular movement. 
In some cases the positive discharge is clearly primary and 
the inhibitory loss is secondary, in others the loss is primary 
and the luminous discharge is secondary. In the former the 
bright spectrum usually surrounds the area of dimness of 
sight; in the latter the primary (or simultaneous) dimness of 
sight extends to the edge of the field of vision and the dis- 
charge occurs within it. 

Besides these two distinctions another is constituted by 
the relation of the symptoms to one side or to both sides of 
the conjoined fields. The double field, of course, extends 
equally on each side of the central fixing-point. In one class 
the leading element is central, and develops around the fixing- 
point, extending on each side of it. In the other, far more 
common, the phenomena alike of discharge and arrest of 
action occur in one half of the field of vision. 

It is not easy to conjecture in which visual region these 
processes occur, Avhether in the lower half- vision centre or 
in the higher. The one-sided symptoms seldom pass beyond 
the middle line, and this fact, together with the simple char- 
acter of the sensations, may suggest that the process for them 
occurs in the lower centre. The pain which folloAvs is on 
the side on which the central function is distributed, that is, 
on the side of the head opposite to that to which the visual 
sensations are objectively referred. If these seem to occupy 
the left half of the field of vision the pain usually begins on 
the right side of the head. But the symptoms which begin 
around the fixing-point, and extend equally on each side, 
can hardly be due to a process in one half-vision centre. 



22 VISUAL SENSATIONS. 

If we assume its seat to be the higher visual centre, it is 
difficult to understand some of its features except by assum- 
ing that both hemispheres are similarly -involved. We shall 
see this better presently. If it seems difficult to conceive an 
actual identity of functional derangement in the two lower 
centres, we may remember the fact I have just mentioned, 
that an irritative lesion in one may cause complete transient 
inhibition of the other. We may remember also that in all 
vision there must be perfect combined action of the two. It 
is certain that the visual impulses first reach these lower 
centres and that neither receives impressions from beyond 
the middle line (except just around the fixing-point) and yet 
there is perfect blending of the two half fields. Although 
conscious vision must be due to the higher sight centres, the 
facts seem to show a perfect unity of function in the two 
sides which lessens the difficulty of conceiving that a similar 
unity should exist in functional disturbance. At the same 
time, the correspondence in feature between spectra that are 
on one side and those that involve both makes it difficult 
to ascribe some to the lower and others to the higher 
centres. To this question I shall have to return. 



UNILATERAL SPECTRA. 

The most common form of pre-migraine spectrum is that 
which is confined to one half of the visual field. Hence it 
is convenient to begin with these, especially because we have 
such a trustworthy record of those forms in the delineations 
of Dr. Airy.* It is difficult to give exact and convenient 
designations to any of these forms which these spectra pre- 

*I am sorry that the reproductions of these here given are destitute of 
colour, but this feature is given in the plates accompanying this lecture in the 
Ophth. Trans, and in Dr. Liveing's book, while many of his original draw- 
ings are accessible in the library of the Ophthalmological Society. 



THE EXPANDING ANGLED SPECTRUM. 23 

sent, but perhaps that which I am about to describe may 
be termed the expanding spectrum, because expansion is its 
special feature. 

The Expanding Angled Spectrum. 

This was the characteristic form experienced by Dr. 
Airy and the following account of his illustrative drawing 
corresponds to many others which he has recorded. 

A bright stellate object, a small angled sphere, suddenly 
appears in one side of the combined fields. In Fig. 3 A it 
is seen a little to the left and below the fixing-point o. It 
rapidly enlarges, first as a circular zig-zag, but on the inner 
side, towards the medial line, the regular outline becomes 
faint (b), and, as the increase in size goes on, the outline 
here becomes broken (c), the gap becoming larger as the 
whole increases, and the original circular outline becomes oval. 
The form assumed is roughly concentric with the edge of 
the field of vision so far as the lower and outer part of the 
oval is concerned, where the lines which constitute the out- 
line meet at right angles or larger angles. These remain 
large and increase as the oval extends, their number and the 
number of the angles continuing the same. The result bears 
some resemblance to the place of a fortification and hence it 
is sometimes called the '' fortification spectrum." But (as seen 
at e) the upper part of the zig-zag oval presents a remarkable 
difference from the rest. The position of the 'break is to 
leave the extremity of this close to the fixing-point of the 
field (o in all the figures). The expansion above is at first 
less, so that the upper side is flatter, and the angles lessen 
progressively towards the fixing-point. Near this they are 
scarcely to be discerned and at last are represented only by 
one or two luminous spots. When this angled oval has ex- 
tended through the greater part of the half field (e) this upper 
portion also expands; it seems to overcome at last some re- 



24 



VISUAL SENSATIONS. 



sistance in the immediate neighbourhood of the fixing-point, 
although close to it the stability seems too great to be 




Fig. 3. — The chief elements of one of Dr. Airy's coloured drawdngs, reduced 
(Trans. Ophth. Soc). A B C D E F and G represent the successive 
stages as described in the text. In all O indicates the fixation point 
(centre of the field). 



overcome, so that a bulge occurs in the part above, and the 
angular elements of the outline here enlarge (as in f), 



THE EXPANDING ANGLED SPECTRUM 25 

although close to the fixing-point the line remains unchanged. 
After this final stage occurs, the outer lower part of the 
outline disappears. This final expansion near the centre pro- 
gresses with great rapidity, and ends in a whirling centre 
of light from which sprays of light seem flying off. Then all 
is over, and the headache comes on. 

It Avill be noted that this expanding spectrum does not 
enlarge to the full extent of the lateral field. Its expansion 
seems to stop at about the outer third. This is not always 
the case. In one patient an expanding spectrum developed 
from a brilhant spot Avhich appeared near the fixing-point, 
on one side, which enlarged and broke medially so as to 
form an expanding horseshoe, which enlarged until it ap- 
parently disappeared at the extreme edge of the field, for the 
patient said that it "seemed to pass over the side of the head 
to the back" — an instance of the apparent objectivity of a 
peripheral spectrum. In this case the spectrum had not the 
common angled form, but seemed to consist of intersecting 

lines, a cheveux de jrise like that of Mr. B presently 

to be mentioned. Colours — red, blue, yellow — were mingled 
in the lines, but precise details could not be obtained. 

The spectrum of Dr. Airy just described is the most 
intense manifestation that he experienced. It was often 
slighter, presenting only a curve, about a semicircle, ex- 
panding as the other, but remaining thus limited. This was 
farther from the fixing-point than in the more intense form, 
but the upper limb of this also was directed towards the 
fixing-point and presented the same diminution in the size 
of the angles, and their ultimate disappearance near the end 
of the line. 

A curious secondary spectrum was sometimes observed 
towards the end of the process. When the expanding angu- 
lar outhne had attained its maximum, a fresh stellate body 
was observed near the broken extremities, at or about the 
3 



26 VISUAL SENSATIONS. 

spot at which the first commenced and similar in aspect. 
Seen for a short time during the fading of the first spectrum, 
it then disappeared, having the semblance of an abortive 
attempt to repeat the process. 

Colours.— The hues which, in Dr. Airy's experience con- 
stituted the angled outhne, varied in length, and the lumin- 
osity was broken or continuous at their junction; it was 



On Monday 
oLj^a^ens' College 
bf%Ie^^ of the 
Lords agafnst tbe I 
of Queens, kindly < 
of Trinity, undertool 



aftpmoon a meeting w 
11^ it jnrs/iereed ( 
alfcA^ J' -^ pree* v 
1 CbJr^^^^^ Dr. 
sented to act 
tbe paji of Secretary' 



eni 




chaij|Ban, and Mj^TTftts, 
It was decided, that 



'etifion BtSulcI not be oifered for signature to any Memb< r« 
of khe Stajate who are Peers, ^^sh^j^k^^yrfcra, or Meaib^ 
of t le House of Comman9^.»Jiij^ ^^^jugnatii 



oft 



^c tould not be fffQnd in t i€ 
^*i:, others were not of sefficif |1 
• names could pot he dtviphen L 
jer of sigpatores attached to t e 




we: 3 received^' 
Rfj ister of Mem 
etaj ling, and the 

these 01 
PetfeioD exi 
lie follo' 
B Senate 
We, the 
weri present 
following 

taken into consideration 

[Here follow tbe Memorial and the 80 signatures, see 
[v an adverse vote of eigh^ 



Chancellor being one of the seven ) a deciaion was come W 
which prevented the wishes of the Metnorialkts from being 
complied with- 

Fig. 4. 



often bordered by a narrow dark Hne. Many of the angled 
lines presented conspicuous colours, bright red, dark blue, and 
yellow. The colour occupied the whole of one of the lines 
or only part of one. The same colour scarcely ever appeared 
on two adjacent Hnes. Red was followed usually by blue, 
sometimes by white, and often a white hne had, as it were, 
a splash of colour in it. It is curious that green was never 
seen, or at least it cannot have been conspicuous, since it was 



INHIBITION. 



27 



never remembered. The only general fact that can be dis- 
cerned is that the contrast in direction is accompanied by a 
contrast in colour. 

Inhibition. — The loss of sight, in the form of the expanding 
spectrum, is always within the angled oval. Outside the 
limiting line, vision is preserved; within it, vision is lost; at 
first over the w^hole area; afterwards, when the sphere is 
broken and has become oval, the loss is most intense close 
to the limiting fine and becomes less towards the middle, 




Fig. 5. — Expanding spectrum (Dr. .^\iry) seen against a dark background, 
and also half against a light window. The luminosity within the spec- 
trum is seen to be dark, w^hen viewed against the hght. 



as is well shown in Fig. 4. This represents the observation 
by Dr. Airy of the print of a newspaper during the develop- 
ment of the spectrum. The luminous zig-zag is represented 
by the black line. 

But the region of inhibition is also one of subdued dis- 
charge. When seen in the dark, or with the eyes closed, the 
region nearest the limiting line, where the interference with 
sight is greatest, presents a bright scintillation. This is 
shown in Fig. 5 in w^hich the first figure represents the 
aspect as seen against a dark background and in the second 



28 VISUAL SENSATIONS. 

figure, the spectrum, a little larger, is seen, half against a 
dark wall and half against the light of a window. The region 
in which the light is dimmed is luminous when viewed 
against a dark background. 

More careful scrutiny of this region of faint luminosity 
shows, as depicted in Fig. 3, that in it there is a peculiar 
linear appearance; lines of luminosity are ranged parallel to 
the segments of the limiting spectrum, most distinct near to 
it. They have somewhat the semblance of internal reflec- 
tions of the lines, becoming nearer and fainter as they recede 
from the limiting line, and they are more conspicuous in 
relation to some of the limiting lines than to others. Un- 
fortunately they seem beyond our present power of inter- 
pretation. 

THE PROGRESSIVE SPECTRUM. 

An angled spectrum may develop progressively through 
a concentric zone of the half-field, in the position occupied 
by that just described when fully expanded. If w^e divide 
each half-field into three zones, central, middle, and outer, 
the spectrum has its seat in the outer part of the middle 
zone. I have only obtained one precise description and de- 
lineation of this form. The angular character is marked, 
but is complex. It develops by progression instead of by 
expansion, and with this we may connect another note- 
worthy fact, that the inhibition of function, causing loss of 
sight, is outside the spectrum and not in it. 

In the patient (Mr. B. already mentioned) who has fur- 
nished the illustrations, the spectrum was in some attacks 
in the right half- field, but more often in the left, as depicted 
in Fig. 6.* The first thing noted (I) was a zone of darkness, 



* I regret that the black-and-white reproduction very imperfectly 
represents the original. 



THE PROGRESSIVE SPECTRUM. 29 

in the periphery of the lower part of the field, diminishing 
inwards. Then, on the inner side of this, a small star or 
angled sphere appeared for a minute or two. As it vanished, 
there developed above it a series of fine angular lines of 




[I IV 

Fig. 6. — Progressive spectrum (Mr. B.). For description, see text. 

light, intersecting each other, and progressing in an arc, con- 
centric with the edge of the field, through about a third of 
a circle. Sometimes the progress of the band of intersecting 
zig-zags would be interrupted by a flash-like line (II). The 



30 VISUAL SENSATIONS. 

chief development occurred in the upper part of the half- 
field (although the initial star was in the lower part). Here 
the intersecting hnes constituted the broadest part of the 
band and in some of the spaces small circles of hght ap- 
peared. In this part also colours were faintly perceived, red 
and blue, in the intersecting lines. Within the curve, espe- 
cially below, much fainter intersecting lines were seen, form- 
ing a zone, which had some analogy to the luminous hnes 
within the expanding spectrum described above as presenting 
the similitude of a reflection. The lower part of the spec- 
trum (first developed) then slowly faded, the upper part 
remaining bright although narrower. As this began to fade, 
a fresh development downwards took place, the first indica- 
tion of which is seen by the downward fine in III. This 
progressed to an extensive development of faint intersecting 
lines in the lower quadrant, as if by an inverted recrudescence 
of the primary process, and it was attended by a progressive 
increase of the peripheral darkness. The brighter region 
above, however, became smaller in area, and finally all faded 
away as intense headache began in the opposite temple. 

Especially noteworthy in this form are the zonular pro- 
gression and the fact that the inhibitory loss was peripheral, 
and began in the neighbourhood of the initial spectrum 
although not in the part in which the chief spectral process 
was seated. There is thus an essential difference between 
these two forms, the expanding and progressive spectra, in 
the relation to them of the loss of function. Yet the differ- 
ence is lessened by the remarkable change in the spectrum 
experienced by Mr. B. The lateral progressive spectrum 
changed to one of pericentral expanding form, still attended 
by peripheral inhibition, but with a central subordinate dis- 
charge. It will be presently described. 



RADIAL SPECTRA. 31 

RADIAL SPECTRA. 

The two forms just described present one common charac- 
ter — the development of the spectra, in their general course, 
is concentric; it presents a definite correspondence with the 
outhne of the field. A marked difference is presented by the 
spectra which have a course from the centre towards the 
periphery, a course which may be termed radial. 

The adjacent figure (Fig. 7) is a representation of a 
diagrammatic drawing made by a patient. An area of dark- 
ness developed in the outer lower part of the field; within 
this was a bright zig-zag of 
uncoloured light. The direc- 
tion of the series of lines is 
radial towards the fixing- 
point, the component lines 
being of course across this 
direction. It is remarkable 
that these are smallest and 
closest together at the pe- 
riphery, and cease before 

reaching the edge of the darkness. It is an illustration of 
discharge within inhibition. 

In another case a similar radial movement was presented 
by a stellate object which remained unchanged throughout. 
It appeared usually near the edge of the right half of the 
field just below the horizontal Hne, and consisted of about 
six pointed leafiike projections, alternately red and blue 
(another example of contrasted colours in adjacent elements). 
It appeared on a small area of darkness, as shown in Fig. 8, 1. 
This stellate body moved slowly towards the left and up- 
wards, passing above the fixing-point, to a little beyond the 
middle line, then it returned to its starting place, retraced 




32 



VISUAL SENSATIONS. 



this path once or twice, and then passed to the right edge 
of the field, keeping in the same direction, so as to come 
near the edge of the field at the lower outer part. Then it 
passed back again, only to a little beyond the spot at which 
it appeared, and then returned to the edge; after two or 




Fig. 8. — Mobile stellate spectrum (see test) 



three repetitions of the last course it suddenly disappeared 
at the spot at which it commenced. The patient kept the 
eyes shut during its existence, but on opening them when it 
had gone, always found she could only see in the part of 



[CENTRAL SPECTRA. ^t, 

the field through which the spectrum had not passed. If she 
looked at a face a couple of feet from her she could only see 
the person's ear on her left side, and all that was to the 
right of the ear could not be seen; in only the third of the 
field to the left was there vision. The loss of sight lasted 
about a quarter of an hour, and gradually passed away. It 
is an instructive instance of the relation of the inhibitory 
loss to the region of the field in which the spectrum appears. 
The case shows how the central disturbance, though pri- 
marily unilateral, may pass beyond the medial fine. 

This patient, after suffering from migraine for many years, 
became the subject of epilepsy, the migraine ceasing when 
the epileptic fits commenced. This transition is not infre- 
quent, and that it was really such is shown by the unusual 
fact that the visual prodroma of the attacks of migraine 
became the warning of the epileptic fits, in more rapid 
evolution. 

Hemianopia. — The inhibitory loss of sight, in the case 
last mentioned, passed beyond the medial line; in the other 
cases illustrated the loss occupied only part of one side. 
True hemianopia, complete loss of one half of the field, is 
often described, but I have never been able to satisfy myself 
of the occurrence of loss up to the middle line such as results 
from organic disease. Patients often state that they can only 
see one half of a face at which they look, but when questioned 
it is evidently only the greater part of one half that is lost. 
Partial dimness of one side is all I have been able definitely 
to ascertain, but the subject needs further careful investi- 
gation. 

CENTRAL SPECTRA. 

The spectra and inhibitory loss hitherto considered are 
essentially one-sided. They begin and extend in one half 



34 VISUAL SENSATIONS. 

of the double field, and if they pass beyond the medial line 
it is to a slight degree and in the last stage of development. 
Indeed, the features of the spectrum of Dr. Airy show the 
resistance which the central region seems to present to pro- 
cess of discharge. In some cases, however, the disturbance 
seems essentially central. One example of this was pres- 
ented by a member of our own profession, whose observations 
were made with care and may be trusted. At the fixing- 
point a small round or oval spot of darkness appeared, en- 
larging rapidly and becoming more intense in the center 
Fig. 9, A). ■ It extended most rapidly upwards and down- 
wards, and more slowly laterally, until the dark area of loss of 
sight occupied the whole medial third of the conjoined 
fields, as simple loss. Its edge on each side presented the form 
of a double curve (Fig. 9, B). It thus caused blindness, ob- 
jects being seen only in the unobscured outer side of each 
field. It often remained thus, without change, until, with 
the onset of the headache, it passed away. Such a central 
loss, so perfectly symmetrical, seems inexplicable by an 
assumed disturbance of the function of one hemisphere. It 
can only be explained by a simultaneous inhibition of the 
structures in each hemisphere related to central vision. Just 
as they must co-operate perfectly in normal sight, producing 
a unity of effect, so we can conceive that they may undergo 
simultaneous functional inhibition, perfectly symmetrical. 

But in this case, on many occasions, the course of the 
central loss was varied by a remarkable and instructive com- 
plication. When the central spot of inhibitory darkness 
had extended through about the middle third of the vertical 
dimension of the field (Fig. 10, A), it became limited on one 
side or the other, but always only on one, by a bright zig-zag 
line of light. This is seen in Fig. 10, B (where the whole 
field is dark because the distress compelled closure of the 
eyes). The line sharply bounded the central blackness on the 



CENTRAL SPECTRA. 



35 



left side. It was an angled white line of light, without colour, 
but with a narrow black edge on each side. As the central 
cloud increased, the bright limiting zig-zag increased in length, 





Fig. 9. 




Fig. 9. — Medial inhibitory loss of sight, before headache, beginning as a 
spot around the fixing-point (A), and then extending from the top to the 
bottom of the double field (B). 

Fig. 10. — From the same case. A. Central inhibitory loss around the fixing- 
point in the double field. On account of the distress caused by it the 
eyes were closed, but the central blackness was still distinct on the dimmer 
background, and became limited by a zig-zag fine of light (B). This 
increased in brightness and width, the angles remaining Httle changed (C). 
A limiting line of greater darkness was distinct on each side of the line of 
light, and the inhibitory darkness extended farther towards the opposite 
side of the double field. 



36 VISUAL SENSATIONS. 

passing below to the other side of the middle hne, but it 
did not move outwards much beyond the place at which it was 
first perceived. It seemed as if the discharge constituted an 
obstruction to the further extension of the inhibition, while 
on the other side the loss of sight spread rapidly, further 
than it did if there was no bright discharge, and almost 
reached the extreme edge of the field. The resistance on 
one side seemed to cause the inhibition to spread farther 
on the other side, and we must perceive in this the intimate 
co-operation of the two hemispheres. Whenever the limiting 
bright spectrum appeared, the headache which followed was 
always on the side opposite to that to which the spectrum 
was referred. We may thus assume that the pain was on 
the side of the hemisphere chiefly in the process of discharge. 



PERICENTRAL SPECTRA. 

A luminous spectrum seems never to develop at the fixing- 
point itself. The nearest approach to it is the development 
of an angled circle around the fixing-point. A coloured zig-zag 
around the object at which he was looking was occasionally 
experienced by the man Beck, and his description and draw- 
ings of this are so precise as to be evidently trustworthy in 
general features. When sitting down to dinner, the zig-zag 
spectrum, coloured red and blue, suddenly appeared, sur- 
rounding the edge of the plate before him. The quaint 
description he gives of it is: "I remember well the phe- 
nomena appearing on the plate when I sat down to dinner. 
As I looked curious my wife said, ' Why do you not carve ? ' 
On taking my eyes off the plate I said to them, ' The zig-zag 
rainbow colours are gone out of the window. This was the 
first time my wife and friends believed I saw something very 
extraordinary." One of his drawings shows the coloured 
angled spectrum surrounding the edge of the plate, and 



PERICENTRAL SPECTRA. si 

another the same circular spectrum in a pane of the window 
at which he looked up. Concentric with the plate as first 
seen, it maintained the same form when he raised his eyes 
to the window, and then disappeared. This fact is more 
important than may at first sight appear, because the form 
of the spectrum was evidently determined by the actual 
stimulation of the visual centres. 

A change in the essential character of the spectrum is 
rare, but, in the case of Mr. B. (as already mentioned) the 
unilateral progressive spectrum, shown in Fig. 6, has under- 
gone transformation with one of the pericentral expanding 
type, a rough illustration of which is given in Fig. ii. The 
fact is of great interest and importance. The first symptom 
of an impending headache is a darkness in the lower part 
of the double field, which ascends to the central region so as 
to cause there a cloudy dimness, so that a large object is 
seen only in parts, which are constantly changing. Then 
the darkness below lessens, as it simultaneously develops 
round the entire periphery of the field. At the same time a 
small bright circle of angled lines appears around the fixing- 
point, and at the same time the central cloudiness disap- 
pears. The angled fines are irregular, but equally so in the 
whole circle. They present no progressive change as in the 
expanding spectrum of Dr. Airy (in which the angles of the 
broken oval lessen in the limb directed towards the fixing- 
point). This bright angled circle steadily expands until it 
ultimately occupies more than the middle third of the field, 
measured from side to side. Its shape being nearly circular, 
it is nearer the top and bottom than the sides of the oval 
double field. Between it and the darkness which lines the 
edge of the field, is a zone in which vision is preserved, 
which peripherally passes gradually into the bounding dim- 
ness, but extends centrally up to the luminous circle. Soon 
after this is perceived, as it enlarges, the area within it pre- 



3^ 



VISUAL SENSATIONS. 




Fig. II. — Pericentral spectrum of Mr. B described in text. 



PERICENTRAL SPECTRA. 39 

sents a luminosity which constantly changes, but presents a 
definite character as the circle becomes large. In spite of 
its mutability, a series of vertical and transverse lines can be 
discerned, leaving between them small squares, spaces occu- 
pied by small circles of light. It must be understood that 
this is only the impression produced by the changing kaleido- 
scopic spectrum. The interest of this feature is the greater 
because similar luminous circles were a feature of the earlier 
one-sided spectrum, seen in the interspaces of the intersecting 
cheveux-de-jrise lines. They were contained by diagonal in- 
tersecting lines in the unilateral progressive spectrum, but 
they are contained by the rectangular lines within the central 
expanding spectrum. 

Ultimately this peculiar central luminosity disappears; 
the peripheral darkness becomes less, the angles of the circle 
become larger and larger, and at last are broken, and it dis- 
appears. The darkness around the field passes away first 
at the sides and lasts longest where it began, below. With 
the disappearance of the spectrum the headache comes on, 
which, strange to say, is still unilateral. 

A spectrum in the form of an arch, in the mid-position, 
above the centre, was also a frequent experience of Beck, 
and may be regarded as a segment of a pericentral spectrum. 
He has given a representation of this, in his usual objective 
style, of which the adjacent figure (12) is a reproduction. In 
another drawing it has become divided in the middle, with 
further loss of some of the constituent colours on each side. 
It is of great interest that the pericentral spectrum of Mr. 

B. (Fig- 11) has lately been limited to the upper half 

of that represented, a semicircle but with the same inter- 
secting lines and circles. In these forms also we are com- 
pelled to think of the perfect co-action of the two centres. 

A form of this arched spectrum was described by another 



40 



VISUAL SENSATIONS. 



patient as a sort of angled crown above the eye. It is an- 
other instance of the tendency to regard these spectra ob- 
jectively. The patient was a member of our own profession, 
.and, in response to my request for a drawing of the aspect 
the spectrum presented to him, he sent me an objective 







Fig. 12. — Arched spectrum (with the colours of the rainbow) as represented 
objectively by Beck. 



representation of his eye with the spectrum above it, in the 
position in which it could, of course, only be seen by another 
person. This involuntary sense of objectivity is a very 



VISUAL SENSATIONS IN EPILEPSY. 41 

curious feature. It is especially strong when the spectrum 
is at the periphery, in the part of the field where vision is 
least distinct. It may be that a vivid sensation, where sensi- 
bility is relatively dim, seems so anomalous as to appear 
absolutely objective. 

These descriptions of the leading varieties of the mi- 
grainous spectra may at least serve to point to the features 
to which observation may be usefully directed. The slower 
development of the symptoms enables much more careful 
observations and more precise record than in the case of 
the very rapid and brief spectra which precede epileptic fits, 
to which we now pass. 



//. VISUAL SENSATIONS IN EPILEPSY. 

A visual sensation or visual loss is common as the imme- 
diate warning of the onset of an epileptic fit — that is, the 
first effect on consciousness of the cerebral process. Loss of 
sight, observed as sudden darkness, is always bilateral. In 
epilepsy there is never simple one-sided loss, not even such 
partial hemianopia as occurs before migraine. Indeed, the 
only case I have met with is the case described above, in 
which the star-like object, moving to and fro obliquely, in 
an area of dimness, was the premonition of the attacks of 
migraine and also the warning of the epileptic seizures which 
afterwards replaced the headaches. 

Some positive visual sensation is, however, a common 
warning. Such sensations are very varied, but they are, as 
a rule, constant in character in the same patient. They may 
be quite simple, as simple as those which precede migraine, 
but they never present the peculiar angled form which is so 
common before headache. They are, moreover, extremely 
rapid in evolution, and brief in duration. Just as the epi- 
leptic fit occupies fewer minutes than the hours during which 



42 VISUAL SENSATIONS. 

the headache lasts, so the warning sensation occupies fewer 
seconds than the minutes during which the visual premoni- 
tion of migraine continues. 

The simplest forms are as follow: (i) A sudden appear- 
ance of a light or colour, compared sometimes to a flash, 
sometimes to a slower glow. It is usually general, but occa- 
sionally seems to occupy part of the field, upper or lower. 
Strange to say, it is seldom seen on one side. An example 
of this has been already mentioned; the uniform warning of 
every fit was the appearance of green through lower part 
of the field of vision, from side to side, spontaneously de- 
scribed as if the patient was "standing in a field of grass." 
(2) Sparks or stars, small and often numerous. If very 
numerous, they may appear in rapid molecular movement, 
like insects on a pond, such as already described as a feature 
of the secondary discharge of migraine. (3) Sometimes a 
larger luminous object is seen, described as round, not as 
definitely stellate, often coloured. It may be of a different 
colour in the centre and margin; in one instance the con- 
stant aura was a bright spot, blue in the middle and red 
around. In some cases the colour is always the same; in 
one it was brilliant blue and was induced by looking at a 
bright light of any kind. But the colour may change, as 
from red to green. Sometimes a simple light may change to 
some definite objects. A light may move across the field 
or seem to approach or recede. A common form of move- 
ment is circular. A bright light appears and moves round 
and round, either seeming to come nearer by movement in 
an enlarging spiral, or to recede ; after a few revolutions, con- 
sciousness is lost. In one case, in which the revolving light 
approached, as consciousness began to fail and the hght 
to become dim, a most offensive smell was experienced, 
always the same, but indescribable. Such rotation seems to 
be a sensory analogue to the form of vertigo in which seen 



SIGHT AND MOVEMENT. 43 

objects have a similar circular motion. The fact that a 
subjective visionary object may seem to move is of much 
significance and needs special consideration. 



SIGHT AND MOVEMENT. 

The apparent motion of spectral objects illustrates the 
close relation of sensory and motor processes. Any sensation 
on the surface will cause an instant movement of the head 
and eyes in that direction. So will a sound that is heard 
on one side: the head is instantly turned in that direction. 
So an object, seen on one side, induces an instant movement 
of the head and eyes towards it, so as to bring it to the 
place of most distinct vision. I remember once seeing an 
instance of this : a number of wild swans, fifty or sixty, were 
floating dow^n a river, when a dog appeared on the bank 
some thirty yards behind them. Instantly every swan was 
in the same position, each neck presented the same curve, 
each head had the same inclination, so as to bring one eye 
of every swan to bear upon the dog. So they remained, in 
the same position, which slowly changed as the dog passed 
by. The correspondence of posture and movement was a 
striking illustration of the uniformity of nervous action under 
the same visual stimulus. In man, in the same way, an 
impression on the retina on one side of the field of vision 
causes an instant movement of the head and eyes towards 
it, to bring its image to the centre of the field. If the object 
moves, the head and eyes follow it. This is true of a sub- 
jective sensation as well as of one that has a real cause. 

There is also an opposite relation between sight and move- 
ment. Not only does sight induce motion, but movement of 
the head or eyes causes an apparent motion of objects that 
are seen. If the image of a seen object occupies the same 
place on the retina, while the head and eyes are moved, the 



44 VISUAL SENSATIONS. 

object must have moved in corresponding direction and de- 
gree. This is an instant inference from the sense of move- 
ment of the head and eyes. But in epilepsy there may be 
such a sense of movement without actual movement; motor 
processes are felt which are insufficient to cause motion. 
From this there results a sense of movement, and a seen 
object, really still, seems to move in correspondence to 
the subjective motor sensation. It is so in other forms of 
vertigo as well as in the epileptic discharge. A sense of 
turning to the right, without movement, induces the impres- 
sion that an object opposite the eyes moves to the right, and 
the individual may be conscious of this impression far more 
than of the motor process which gives rise to it. Thus the 
sense of objective movement may be apparently primary when 
really secondary. 

This is most common and most important in the subjective 
sensation of motion to one side, so frequent in the visual 
sensations of epilepsy. It is related to the deviation of the 
head and eyes which is a common feature of the attack, and 
so often begins it. It must be ascribed to the fact that the 
discharge is greater in one hemisphere of the brain than in 
the other, and when it is the earliest motor symptom, it show^s 
that the discharge on one side develops before that on the 
other. Such turning of the head and eyes to one side is 
not unfrequently associated with a visual sensation. 

If an object actually in motion appears on one side of the 
field, say on the left, the effect of the sensory impression on 
the brain is primarily on the right hemisphere. The visual 
process arouses the motor centres on that side which turn 
the head and eyes towards the left to "fix" the object. But 
the object is moving from left to right, and, therefore, to 
keep the object fixed, the first movement towards the left is 
followed by one in the opposite direction, due to the left 
hemisphere, to follow the object, until it disappears on the 



SIGHT AND MOVEMENT. 45 

right. This long movement to the right is then followed by 
a return movement to the mid-position, by the action of the 
right centre, when the exciting object has disappeared. 

Note this normal alternation under the influence of stimu- 
lation of the visual centre of one hemisphere from the opposite 
side — motor action first in that hemisphere, then in the other, 
and lastly in that which was first excited. Such alternation 
of motor activity occurs in disease as well as in health ; it may 
be associated with a primary discharge in the visual centres, 
causing a visual epileptic aura. 

It may be a useful illustration of what I have said if I 
mention a case in which the same motor sequence occurred 
as a result of an organic lesion, traumatic meningeal haemor- 
rhage over the left hemisphere. It caused a long series of 
right-sided convulsions with strong deviation of the head and 
eyes to the right. But this was preceded by their deviation 
to the left, and before the turning to the left there was initial 
briefer deviation to the right. The slow-commencing dis- 
charge in the left hemisphere, causing this first movement to 
the right, seemed to excite a stronger activity in the right 
hemisphere, with deviation to the left, before the final intense 
discharge of the convulsion with strong deviation to the 
right. The meningeal haemorrhage was over the left hemi- 
sphere only, and the phenomena of the fits, which I watched 
for hours, show the very close connection between the motor 
centres in the two hemispheres, and their disposition to 
alternate energy, such as they manifest in response to visual 
excitation. 

These facts illustrate the features of a case which is 
specially instructive. A boy, at the age of five, had a severe 
general illness, of unknown nature, during which sudden 
hemiplegia came on. Partial recovery was followed by re- 
curring convulsions of the left, hemiplegic side. Each fit 
began thus: a slight movement of the head to the left, a 



46 VISUAL SENSATIONS. 

much stronger and longer movement of the head towards 
the right, then a deviation again to the left, intense, as the 
boy passed into the convulsions, chiefly on that side. Here 
we have again the same sequence, and here we have an 
opportunity of discerning more of the process. The patient 
came under observation as a most intelligent boy of eleven 
years of age, and described the following warning : The figure 
of a man suddenly made its appearance at the extreme left 
of the field, slowly moving towards the right. He felt com- 
pelled to try to look at it and to follow it, and did so until 
it disappeared at the right edge of the field. Then he lost 
consciousness, and knew nothing of the subsequent strong 
deviation to the left in the fit. The movement to the right 
(to follow the object) chiefly impressed his consciousness, and 
was felt as conscious turning to the right. Here, then, we 
have these sequences distinctly associated with the action of 
the visual centre, and, apparently, with the influence of this 
on the motor centre. Yet one other case. In this, each fit 
was preceded by the sudden appearance of a blue hght on 
the left side, sometimes of two or three, near together. These 
always moved slowly towards the right and a little upwards, 
and the patient felt compelled to follow them. The head and 
eyes were moved towards the right in this effort, as far as 
they could be, by strong tonic spasm in the muscles of the 
neck. This occupied about thirty seconds, and then sud- 
denly ceased on the disappearance of the visual spectrum. 
The eyes and head, thus released, could be moved from the 
right, but this movement was continued towards the left as 
an involuntary movement, which was, however, far greater 
in the eyes than in the head. For nearly a minute the eyes 
were turned extremely towards the left, and the head only 
half-way from the mid-position. During this time he could 
move the head towards the right, but was absolutely unable 
to move the eyes from their extreme deviation to the left. 



MICROPSY AXD MACR0P5Y. 47 

Then he lost consciousness and the general convulsion of the 
lit came on. We have here again the same sequence, but the 
compulsion was not left-sided, it was general, and the final 
left-sided deviation of the head had not the intensity which 
accompanies a left-sided fit. I could give other similar 
instances, but these may suflice to indicate the close relation 
of the movement of the head and eyes to acti^'ity of the visual 
centres. I may point out how indispensable, for understand- 
ing the facts, is the theon* of the representation of both fields 
in the higher ^-isual centres and of their mutual action. 

An apparent motion of spectral objects upwards or down- 
wards as part of the \'isual aura of epilepsy seems to be ex- 
tremely rare. I have not met T\^th it. An apparent rotation 
of objects actually seen is often described as a feature of 
initial vertigo, but this is not \\dthin our present subject. 
^lovement in circles has been already mentioned. 

Micro psy and Macropsy. 
An apparent movement towards or from the subject is 
not uncommon in the case of spectra, and even of objects 
that are actually seen. I have already mentioned this 
fact. Recession is usually associated ^dth diminished size 
and sometimes with dimness of sight, but of the pa- 
tients I have questioned, a few have been sure that the 
apparent recession of seen objects was not the result of 
their dimness. It may be due to a central condition re- 
lated to diminished convergence and accommodation. But 
such a recession is rarely described in the case of subjective 
sensations. With these, apparent approximation is the rule. 
A spherical fight, for instance, seems to get nearer and larger 
until it overwhelms the patient as consciousness vanishes. 
It is noteworthy that such approximation is described only in 
the case of simple ^'isual sensations, not in those of elaborate 
character. 



48 VISUAL SENSATIONS. 

Psycho-visual Sensations. 
More elaborate sensations often constitute the warning of 
an epileptic attack, but are unknown in association with 
migraine. They are definite sensorial conceptions of figures 
of persons, or faces or scenes. A simple luminous object 
may change to such, as already mentioned. These are so 
much higher in the scale of mental processes than the simpler 
sensations already described that they may be termed ''psy- 
cho-visual." I have given many instances in my book on 
''Epilepsy."* It is remarkable that the visual conception, 
however elaborate, is generally constant, preceding every 
attack. It may be such as cannot have been within preceding 
experience. In one patient, for instance, every attack was 
preceded by a sudden vision of London in ruins, herself the 
sole survivor in the scene of desolation. 

Associations. 
Visual sensations may be associated with subjective 
sensations of hearing, very seldom of smeU. The two are 
often of the same degree of elaboration. If the vision is of 
a person, words may seem to be heard, although they can 
seldom be recalled. One strangely complex aura, which pre- 
ceded every fit the patient had, deserves mention. It began 
in a simple form. First the beating of the heart was felt, 
and this ascended the chest to the head, where it seemed to 
become audible as a sound; then two lights appeared before 
the eyes and seemed to approach by jerks, synchronous with 
.the pulsation. The lights then disappeared, and were re- 
placed by the figure of an old woman in a red cloak, who 
offered something that had the smell of Tonquin beans ; then 

* " Epilepsy," etc., second edition; London, ChurchiU's; Philadelphia, 
Blakiston's; 1901. 



ASSOCIATIONS. 49 

consciousness was lost. The case is remarkable on account 
of the change of the sensation of simple pulsation to that of 
sound,* the association of the latter with a pulsating visual 
spectrum, the replacement of these by a highly complex vision, 
and the final termination with an olfactory sensation, probably 
elaborate. The jerky movement, definitely synchronous with 
the pulse, is not uncommon in such simple visual sensations, 
and seems to indicate that the process, in the disturbed centre 
of the brain, is modified by the mechanical influence of the 
arterial pulsations. I may point out also the interesting fact 
that the more elaborate sensation, the vision of the woman, 
followed the more simple one, the two lights. This sequence 
is more common than the opposite, although now and then 
an elaborate sensation is followed by one that is more simple. 

I have mentioned a case in which a light, approximating 
by circular movement, was associated with an offensive 
smell. I have met with other instances in which an un- 
pleasant olfactory sensation was associated with a simple 
visual sensation, and an agreeable smell with one of complex 
character. 

I have already mentioned the remarkable fact that the 
sudden spontaneous activity, which we call "discharge" of 
the centre, is often preceded by sudden arrest of function, 
by inhibition. It is one of many instances of the fact that 
the same functional derangement, in different degree, seems 
to cause cessation of action or increased action. In one case, 
suddenly all became dark, then there appeared a red hght 
before the eyes, changing presently to green, and then con- 
sciousness was lost and the convulsion came on. In another, 
sight became dim and misty, then two round green lights 
appeared, compared to a penny at a distance of two feet; 
these moved from side to side. It is very common for the 

* See the following lecture, on "Subjective Sensations of Sound." 
5 



so 



VISUAL SENSATIONS. 



first darkness to be the background for bright stars. In these 
cases there is discharge in a centre first inhibited. Much less 
frequently, stars or flashes of light are followed by loss of sight 
and darkness, — that is, discharge is followed by inhibition. 

///. MISCELLANEOUS SENSATIONS. 

Spontaneous activity of the visual centres, giving rise to 
a sudden light, or colour, or to the impression of some seen 
object, sometimes occurs in abnormal cerebral states apart 
from epilepsy or migraine. But such visual sensations are 
too rare and too vague in their associations to merit detailed 
description. As an instance of the anomalous visual im- 
pressions that may occur, may be mentioned the case of a 
woman, aged thirty-seven, who frequently experienced a 
peculiar colour hemiopia; if one eye was closed and a light 
was looked at (as a candle-flame) the temporal half appeared 
blue, the nasal half normal. Some time afterwards only a 
bluish-purple halo appeared all round the flame. After read- 
ing for a few minutes the page of print appeared a light 
green, and then changed to lilac or pink, and then these 
colours became mixed and mottled over the page. On rest- 
ing the eyes, sight became normal, but a few minutes after 
resuming reading the same colour phenomena occurred. No 
abnormal condition of the eyes or field could be found. 

Vertical Hemianopia. 
The blending of the visual centres in the two hemispheres 
is strikingly evident when subjective functional disturbance 
has a distribution, not from one side, but in the vertical direc- 
tion. I have mentioned one instance of this, in which the 
aura of epileptic fits was the sensation of a green colour 
throughout the lower half of the visual field. The impression 
was spontaneously compared to "standing in a field of grass. " 



CONCLUSIONS. 51 

In very rare cases the lower part of the fields is lost before 
migraine, the division being either transverse or obhque. In 
one case it was preceded by numbness in the upper lip. 
Coloured zig-zags were sometimes seen, but not on the 
occasions of the transverse loss. In the oblique passage of 
the stellate spectrum just described (Fig. 8) we have evi- 
dence of a functional disturbance involving both sides of the 
double fields, which makes it easier to realise that the dis- 
turbance of the centres may have such a form as to cause 
inhibition of the upper or lower regions. In the cases I have 
met with the loss has been in the lower half. 



CONCLUSIONS. 

Far more observations, precise and detailed, are needed 
to enable any definite inference to be drawn regarding the 
indications of the phenomena that have been considered. 
Indeed, it is probable that, for a long time, the chief result 
of more observation will be to point the line in which still 
more is needed, if real knowledge is to be secured. Frequent 
as is migraine, and frequent as are the associated visual 
spectra, the ability to observe carefully such quickly changing 
phenomena is rare, and their combination with mental dis- 
tress constitutes a further hindrance. Still more rare is the 
ability to depict them, and even to describe them with needful 
precision and fulness. But the example afforded by Dr. 
Airy, who has added so much to our knowledge, should not 
be lost on the many members of our own profession who' 
are similar sufl'erers. We may learn much regarding the 
action of the cerebral centres from such observations. The 
features of the spectrum in character and colour, its progress, 
its initial form, position and development, the way and place 
at which it disappears, are each and all important. So also 
are the precise position and relation of the colours that appear. 



52 VISUAL SENSATIONS. 

Not less important is the relation of the positive spectrum to 
the inhibitory darkness. 

Yet the question presents itself again and again, to what 
part of the visual centres are these phenomena to be referred ? 
The problem has been already referred to, but we may note 
that one conclusion seems compelled by a consideration of 
the phenomena — they must, in most cases, depend on a func- 
tional fusion of the centres in the two hemispheres. This is 
obviously the case if they can be regarded as due to a dis- 
turbance in the lower half vision centres, and it is equally 
necessary if we assume that the higher visual centres are the 
seat of the disturbance — the assumption on which they are 
best explained. 

We have seen that the indication of loss of function is that 
each higher centre is able by itself to subserve vision in a 
large area around the fixing-point in the opposite eye, having 
a diameter of about a third of the field, and of a much smaller 
area in the eye of the same side, having a diameter of about 
one-eighth of that of the field. In the rest of the fields vision 
depends on the combined action of both visual centres. The 
two hemispheres, acting together, subserve vision up to the 
periphery of the field. (How real is the mutual co-operation 
of the two hemispheres is shown by the facts regarding the 
augmentation of colour- vision mentioned on page 14.) The 
inference from these facts is that the intensity of functional 
action in the combined centres lessens from the centre to the 
periphery. If we divide the double field into three zones, 
each limited at a third of the radius : wx have a central zone 
around the fixing-point (subserved by the opposite hemi- 
sphere acting alone), a larger middle zone, and an outer 
peripheral zone. The chief development of the expanding 
spectra seems to occur in the middle zone. This division may 
at least serve to guide future observations and make them 
more precise. 



CONCLUSIONS. 



53 



I 



The difference between the two forms of expanding spec- 
trum, the one-sided oval of Dr. Airy and the pericentral 
later form of Mr. B., suggest that in the former the discharge 
is in the higher centre of one hemisphere, while in the latter 
it occurs in both, combined by a perfect functional fusion. 
In the former the first stellate object appeared on one side 
of the fixing-point, near to it; in the latter, the initial small- 
angled sphere was around the fixing-point. The area imme- 
diately adjacent to the fixing-point seems not to be involved in 
the discharge. The centre for this, the area of acute vision, in 
either hemisphere, seems to possess an invincible resistance 
to primary discharge ; although it may undergo inhibition and 
secondary subactivity. 

On the other hand, the peripheral part of the fields, 
which seem to need the co-operation of both hemispheres for 
vision, may undergo arrest of function in association with the 
zonular discharge. It seems to be an associated event, and 
not a consequence, since it may come first, and is most 
intense at the edge of the field, lessening towards the spectral 
zone. 

Inhibition within the area of discharge is met with only in 
the expanding form, and seems a residual derangement of 
the structures through which the discharge has passed, by 
which they are the seat of subordinate activity with an ina- 
bility to receive the impulses that reach them from without. 
It is a derangement which, intense when the discharge has 
just passed (causing the semblance of reflection presented 
in Dr. Airy's drawings. Fig. 3), lessens gradually. In the 
pericentral spectrum of Mr. B. (Fig. 6) the features of the 
subordinate discharge within it are remarkable; their uni- 
formity in the enclosed area may be connected with the 
fact that it is the central region of the field. But the most 
remarkable relation of discharge to inhibition is the limita- 
tion of medial darkness by the spectral barrier shown in 



54 VISUAL SENSATIONS. 

Fig. lo. It is a striking illustration of secondary discharge. 
The inhibition extended from top to bottom of the double 
fields, perfectly symmetrical, and can only be conceived 
as an arrest of action of the combined centres in the two 
hemispheres, practically one. Often it remained symmet- 
rical medial darkness, until it passed away. Sometimes 
on one side, presumably in one hemisphere, when the inhi- 
bition had almost reached its limit, the process suddenly 
changed to discharge, a bright zig-zag, hke a hghtning-fiash 
at the edge of a thunder-cloud. The discharge continued 
fixed, as an absolute limitation to the arrest on that side, but 
it spread still further on the other. It seems as if the 
process that was going on uniformly in the conjoined centres 
of the two hemispheres suddenly gave place to discharge in 
one. It is remarkable that the discharge was limited to the 
side on which the later pain was felt. 

The examples of spectra which proceed in what I have 
termed a radial course, from the edge of the field towards 
the middle, are too few to permit any inference from their 
remarkable features. These present a contrast to the spectra 
of concentric form. They occupy the peripheral region, into 
which the latter do not pass. But it is notcAvorthy that the 
discharge seems to be always within a region of inhibition, 
and that movement is in opposed directions, so as to produce 
either a series of close-angled lines, or the aspect of an object 
moving backwards and forwards. Our need is especially 
great for more observations of spectra of this class. 

The close relation between inhibition and discharge is 
conspicuous in most of these phenomena. The process of 
arrest seems to be a slighter degree of that which causes 
excessive activity. This is conceivable even though they are 
exactly opposite in nature. If we consider the processes in 
the light of the neuronic theory, and the dendritic endings 
as the source of the nerve impulses, we can conceive that a 



CONCLUSIONS. 55 

slight degree of energising may induce their retraction, with 
inaction as a result; a greater degree of functional activity 
may cause the impulses to burst through the intermediate 
substance and induce the approximation of the dendrites in 
intense action. Certain it is that the relation between arrest 
and activity is common in all such spontaneous processes. 
In a shght epileptic fit, due to local disease, the arm may 
fall powerless, while in a more severe attack it is violently 
convulsed. So, too, also in epilepsy, sudden darkness may 
be followed by bright lights. The mobile star or zig-zag 
just mentioned, within the area of darkness, illustrates the 
same phenomena. 

These processes, as discerned and presented in the field 
of vision, have to be described in topographical language. 
We know that such description is accurate as regards the 
lower visual centres. We know that destruction of a definite 
part of this centre causes loss of a definite part of the half- 
field it subserves. But we are not justified in assuming any 
topographical correspondence of the higher visual centre to 
the visual field. On the contrary, present evidence suggests 
that partial damage lowers the action of the whole, and that 
function is subserved in it in a way to which we have as 
yet no clue. If so, we must obtain far more knowledge before 
we can hope to understand the precise features of the spectra 
described, such as the contrasted direction of the lines and 
their contrasted colours, which compose the spectrum, 
whether the lines are continuous or intersecting, — the precise 
position of the spectrum in relation to the double field, and 
especially its relation to the fixing-point in its origin and 
course. Not less important is the position and development 
of the area of darkness. In the hope that more facts may 
be forthcoming, I w^ill conclude with a simple diagram of 
the double visual fields, which can be easily copied or en- 
larged, on which can be depicted the phenomena observed. 
The form of the discharge can be indicated by pencil lines, 



56 VISUAL SENSATIONS. 

the area of inhibitory darkness by shading. If a wash of 
colour is put over it, the bright spectrum can be indicated 
by scratching off the colour with the point of a knife, and the 
darkness by shading. An indication of the colours seen, 
and their position, would add much to the value of the 
depiction. I hope that from the many who suffer and 
have the ability to supply the record, some facts may be 
furnished which will enable us better to understand that 
which is now mysterious. We cannot tell what additions to 
knowledge may result from facts that seem simply curious. 
The information regarding the cerebral visual functions 
furnished by organic disease is chiefly negative; it is almost 
limited to their loss. Only in such functional disturbance as 
we have considered have we evidence of active functional 
disturbance. Deranged though it is, we must learn from it 
much that can be discerned in no other way, and may learn 
more than we may anticipate. The phenomena seem mys- 
terious, but we cannot doubt that the mystery will lessen as 
observations accumulate, careful and precise. 




Fig. 13. — Outline of the double field, to be enlarged for the depiction of 
spectra. The star is in the position of the fijxing-point. If this is re- 
placed by a small hole, looked through while the diagram is held near 
the eye, the relation of the spectrum to this can be best discerned. 



LECTURE II. 

SUBJECTIVE SENSATIONS OF SOUND. 

THE BRADSHAW LECTURE, 

Delivered before the Royal College of Physicians of London, November s, iSg6. 



I had an opportunity, not long ago, of considering the 
sensations of sight which occur apart from external cause, — 
subjective visual sensations. I propose to take the present 
occasion, afforded me by the honour of the delivery of the 
Bradshaw Lecture, to consider the analogous sensations of 
sound, — subjective auditory sensations. Between the two 
we may trace some points of resemblance and many of dif- 
ference; but the sensations of hearing merit, not less than 
those of sight, a careful study. This indeed they have many 
times received in their relation to the ear, but their general 
features, especially in relation to the brain, have had less 
notice. The relations of these symptoms to the sensory organ 
itself are far more obtrusive in the case of the ear than the 
eye. Ocular disease rarely causes symptoms of this char- 
acter, whereas they are among the most common and most 
distressing effects of disease in the ear. This has been recog- 
nised by terminology, popular and medical. "Xoises in the 
Ears" and "Noises in the Head"; "Tinnitus aurium" and 
"Tinnitus Capitis" — these terms express the prominence to 
which the symptoms attain. 

We speak of these sensations as "subjective" because 

6 ^7 



58 SENSATIONS OF SOUND. 

they have no external cause, — no cause such as normally 
gives rise to a sensation of sound. But many of them have 
a definite cause, external to the structures in which the 
auditory nerve ends, although not external to the ear itself. 
Of those that have not such causation, many are due to 
processes in the structures of the labyrinth in which the 
auditory nerve ends, and through which the waves of sound 
excite nerve impulses. Others again arise by a morbid func- 
tional action of the centres in the brain through which the 
impulses from the auditory nerve affect consciousness, and 
these are subjective in the purest sense of the w^ord, while 
a few are perhaps due to disturbance at some point in the 
intermediate conducting path. The subject is thus highly 
complex. I think I may best present to you its chief outlines 
if I confine myself to the facts regarding the several forms 
that have come under my own notice. This limitation does 
not imply any assumption of originality on my part. I 
doubt not that many things I have to say have been said 
before, and to those by whom they have been said I owe 
this explanation; but it is curious how few attempts have 
been made to consider these phenomena systematically. 

Afnong the facts that I shall have to mention are some 
relating to the power of hearing certain musical notes. These 
are usually indicated by a number for the octave attached to 
the letter of the note. They may also be indicated by the 
number of vibrations a second.* For the production of the 
notes, tuning forks are available up to C^, and above this 
we have that most useful aid to clinical observation, a Gal- 
ton's whistle. By this, high notes can be produced with pre- 
cision, ranging from 4,000 vibrations (two octaves above the 
treble clef) to the utmost capacity of the human ear, 20,000 



* TMs is considered, and the most convenient system suggested, in a note 
appended to this lecture. 



VISUAL AND AUDITORY SENSATIONS. 59 

or 25,000 vibrations a second, and, indeed, far higher, when 
a cat will start though there is absolute silence to us. Age 
lessens the power of hearing these high notes, but the sig- 
nificance of a deficiency that is either early or one-sided is 
definite, and renders the service of this instrument in diag- 
nosis very great. 



Visual and Auditory Sensations. 

The resemblance which exists between the subjective sen- 
sations of vision and those of sound is superficial; the dif- 
ference is profound, and it is also instructive. Subjective 
visual sensations are chiefly of central origin, and in them- 
selves are chiefly of physiological interest, while those of 
hearing are to a large extent produced in the sensory organ 
itself and are often evidence of its disease. They are often 
so obtrusive, and even distressing, that by the sinister dignity 
of the special name, tinnitus aurium, the symptom has 
almost come to be looked upon as an independent disease. 
A definite designation is, however, at least a testimony to 
the frequency and reahty of the suft'ering that is caused. It 
would be harmless w^ere it not that names, once called into 
existence as our servants, are never long content with servi- 
tude. Too often we find ourselves controlled by them, and 
that which is only a symptom, when it has been named, 
is often looked on as an actual malady. 



Sight and Hearing. 

The frequency with which the ear, compared with the 
eye, is a cause of subjective sensations, is also of indirect 
significance. We are apt to place these two senses too 
near together in our thought. Both are indeed excited by 
energy in the form of wave motion. Hence they present 



6o SENSATIONS OF SOUND. 

points of resemblance which may attract more attention than 
does the difference, or rather the contrast, between them. 
Consider, — for the question is of importance for us, — con- 
sider the difference involved in the frequency of the vibrations 
that act on each organ. If we take a colour about the middle 
of the visible spectrum and a musical note below the middle 
of the treble clef, we shall find that, in the interval of time 
between two successive waves of sounds there occur about 
one million million waves of light. The statement seems in- 
credible, but it is true, although, like many other facts, it 
transcends our power of imaginative conception. So does the 
difference in rate of propagation. Light is transmitted about 
one million times faster than is sound in air. It is not sur- 
prising to find, therefore, that whereas the waves of sound 
occur only in media so definitely material that they can be 
weighed, the waves of light occur in a medium which is not 
only imponderable but almost hypothetical. Further, the 
waves of light can be traced upwards until they vanish to 
our direct perception, though beyond them, and their actinic 
successors, there seem to be waves of such a nature that they 
have been designated by the algebraic symbol for that which 
is unknown — the letter x. On the other hand, they pass 
downwards to the slower waves of heat, which we cannot see 
and yet can feel. The waves of sound pass up beyond the 
range of human hearing, though they may still be audible to 
animals. How far higher they extend we do not know. But 
the lower notes of music consist of vibrations so slow as to 
be perceived by the sense of touch if they occur in a medium 
sufficiently inelastic, and at last they can be only felt, ceasing 
to be audible except as a series of sounds not musical. 

With the enormous difference in time between the waves 
of sound and those of light, and the vast difference in the 
character of the media in which they occur, is associated 
another difference. The waves of light, like the common 



SIGHT AND HEARING. 6i 

waves of water, are transverse to the line of propagation 
(''transversal" waves, according to the double adjectival 
form which physicists have revived). But the waves of 
sound are "direct"; they occur in the hne of propagation, 
as the motion between billiard balls when one at the end of 
a row is struck and that at the other end moves off. These 
"direct," or "end-on," waves seem to possess a greater im- 
petus, and such wave motion has a relation to the simple 
motion of a mass; it resembles simple "contact," by which 
the nerves of touch are commonly affected. These facts, 
which point to an essential identity between the stimulus of 
touch and that of sound, are not disturbed in their signifi- 
cance by the special character of many auditory sensations, 
such as musical notes. We may note, moreover, the facts of 
development that show a common (epiblastic) origin for the 
structures that subserve each form of sensation, hearing and 
touch, and the facts of anatomy, which show that sound is 
received by minute hairs that act upon the nerves. We may 
also note the facts of comparative anatomy, which show the 
early form of the ear to consist simply of hairs upon the skin 
connected with a nerve which is homologous with that of 
hearing in higher animals. We shall presently see in other 
ways the importance, for our subject, of this relation of 
hearing to the sense of touch, but I may point out that it 
removes one apparent anomaly — the fact that one part of the 
auditory nerve seems to have nothing to do with hearing. 
Although we cannot say that sound does not act upon the 
structures of the semicircular canals, we cannot doubt that 
their chief function is to cause nerve impulses to be produced 
by the simple motion of the fluid within them, and its varying 
pressure on the hairs in their dilated ends. We have in this 
a response to the very simplest form of motion, quite as simple 
as that which excites the nerves of touch. And I would ask 
you especially to note the fact that, in the same organ, struc- 



62 SENSATIONS OF SOUND. 

tures which closely resemble each other give rise to sensory 
impulses which seem to us quite different, but may prove to 
be nearly related. The impulses produced in the semicir- 
cular canals do not act upon consciousness, although their 
effects may do so. 

Varieties of Tinnitus. 
I may safely assume that the chief features and varieties 
of tinnitus are familiar to you. You know that tinnitus may 
be a continuous sound, or pulsating, and that in the latter 
case the pulsations correspond to those of the arteries. You 
know also how many and extensive are the variations in its 
character, from the simplest to the most elaborate sound, 
from a rushing or roaring sound, or whistling, to that of 
bells, or music. The frequent coincidence of these sounds 
with evidence of ear disease, varying in seat and character, 
but generally involving the labyrinth and often limited to it, 
compel the conclusion that the most common source of these 
sounds is the internal ear, in which the auditory nerve is 
normally excited. But we have cases, especially those in 
which the sensations are the warning of epileptic fits, in which 
we must regard the auditory centre in the cortex of the brain 
as their source, and in rare cases the correctness of this con- 
clusion has been proved by the discovery of organic disease 
in this region. It is strange that we have no evidence to show 
that any part of the intermediate path between the organ of 
hearing and the auditory cortex may be a cause of such sen- 
sations. We should, indeed, hardly expect them to be due to 
a morbid process in the nerve fibres which conduct the audi- 
tory impulses, but the grey nuclei, in which the nerve fibres 
seem to end, might reasonably be thought capable of giving 
rise to impulses which produce, in the centre, the effect neces- 
sary for a sensation of sound. Yet such evidence is not 
forthcoming. 



APPARENT LOCALITY OF THE SOUND. 63 



APPARENT LOCALITY OF THE SOUND. 

Some important considerations are suggested by the com- 
mon name of the symptom — "tinnitus aurium" or "tinnitus 
capitis," — in popular language "noises in the ears" or 
"noises in the head." We may leave for the present the 
reference of the sound to the head itself. The question 
arises: Why is the subjective sound commonly referred to the 
ear and not to the external world? Subjective visual sensa- 
tions always seem of outside origin, why do not those of hear- 
ing? The answer is complex, and brings before us many 
points connected with the subject. The apparent source of 
the sound seems to be, in part, a matter of mental inference. 
Continuous sensations — hissing or buzzing, for instance — 
seem as a rule to be of external origin w^hen they are first 
observed, but their persistence soon convinces the sufferer 
that they cannot be. Knowing that they must have their 
origin in the ear he ceases to refer them to an external cause, 
and they then seem to him to be felt in the ear, although 
often, if he can separate the sensation and the inference, he 
can still for a moment realize that they seem due to some- 
thing outside. It is so, also, with brief unfamihar sounds. 
At first — now and then, indeed, always — they seem to have 
an external cause, but their repetition involves the knowledge 
that they have not, and the knowledge so acts on conscious- 
ness that they seem to be produced in the ear. An instance 
of this was afforded by a patient who was subject occasionally 
to the sound of a bell several times repeated. When he first 
became liable to the sound, in his annoyance, he sent a mes- 
sage to his next-door neighbour asking that the clock might 
be stopped, the sound of which so much distressed him, and 
he only discovered the subjective nature of the sound when 
he was informed that the neighbouring house did not contain 
a single striking clock. Having thus learned that the sound 



64 SENSATIONS OF SOUND. 

could not be due to an external cause, it ceased to seem to 
be. An instance of persistent reference to an external cause 
was a girl subject to a sound exactly like two or three taps 
at the door; in spite of her past experience she frequently 
called out : "Come in. " A woman who had long been liable 
to attacks of a rumbhng sound, each lasting from a quarter 
to half a minute, was never able to distinguish them from 
distant thunder. Even after she had long know^n of their 
subjective nature, she would ask persons near her whether 
they did not hear distant thunder. Elaborate sounds gener- 
ally seem external. 

Pulsating Tinnitus. — On the other hand, pulsating tinni- 
tus is almost always referred to the ear, even from its com- 
mencement. It may be compared by the patient to machin- 
ery and the like, but only as regards its character. The 
mechanism of pulsation in tinnitus is a question of great 
interest, because this feature is common when there is no 
increase in arterial pulsation and when there is no auditory 
hyperaesthesia. It is an instance of mechanical influence on 
nerve function. But the pulsatile element is not only a 
rhythmical interruption in the sound; there is often a char- 
acter which is not purely auditory, although it is only from the 
observation of very intelligent patients that the fact can be as- 
certained. There is a local sensation beside that of sound ; it 
is, perhaps, generally perceptible only as a local character of 
the sound; sometimes, however, it is distinctly a suggestion of 
a pulsating sensation within the ear distinct from that of hear- 
ing. This fact gives importance to other local sensations not 
auditory. One patient with labyrinthine deafness and attacks 
of vertigo had occasionally, as an isolated symptom, a brief 
sensation which could only be described as a "rushing out" 
through the ear, evidently much more a simple sensation than 
a sound. Another patient, a man aged fifty years, with changes 



APPARENT LOCALITY OF THE SOUND. 65 

probably gouty, in the left labyrinth, causing some deafness, 
had a buzzing noise which would occasionally change to a 
throbbing sensation certainly not auditory; and sometimes 
there would occur behind the ear a momentary sensation as 
if the bone were being crushed in, neither pain nor sound. 
These cases show how much we need more facts on this point 
from patients with the ability to observe. I think that there 
must be sufferers among members of our own profession who 
are capable of adding much to our knowledge by careful 
personal observation. 

Rejerence to the Ear. — It is not altogether difficult to under- 
stand such a feature as the local sensation I have referred 
to. We cannot doubt that nerve impulses are continually 
passing from the ear to the brain of which we have no con- 
sciousness. Disease of the internal ear may cause pain. 
Wherever pain may be caused — for instance, by inflamma- 
tion — there must be afferent nerves, however free from sensi- 
bility the structure normally may seem to be. Wherever 
there are afferent nerves those nerves must be in constant 
activity, in some degree. In such an organ as the ear, morbid 
states w^hich act on the auditory nerves may readily produce 
impulses also in nerves that are of different function — im- 
pulses that may act on consciousness. We can feel sure that 
unfelt afferent impulses are constantly produced in the middle 
ear. They must be continuously generated by its muscles. 
The action of at least one of these may cause a strong sensa- 
tion, and the fact can be verified without difficulty. In many 
individuals, probably in all, a voluntary contraction can be 
produced in, apparently, the stapedius muscle. By closing 
the eyes tightly, and then trying to turn the eyeballs up, a 
loud fluttering sensation is produced in the ear, which con- 
tinues as long as the contraction in the face lasts. It is in 
part a sound, but in greater part a simple sensation, evidently 



66 SENSATIONS OF SOUND. 

the result of muscular contraction. A little practice will 
enable those who are sufficiently curious to produce it very 
readily by a mere contraction of the orbiculares.* 

The nerves through which this sensation is produced must 
be constantly excited, without sensation, by the changes in 
the state of the muscles, which, we cannot doubt, are constant. 
A similar fluttering sensation may be a morbid symptom. A 
woman aged fifty-three was liable to occasional attacks of 
severe neuralgic pain in the left side of the head, and when 
the pain was at its height a fluttering in the left ear could 
be perceived lasting five or ten minutes at a time. Moreover, 
she presented an illustration of another association of these 
sensations ; during the severe pain she would sometimes hear 
an occasional loud noise referred to the front of the ear and 
compared to guns going off. There is also some evidence to 
show that a spontaneous contraction in this muscle during 
sleep is the cause of the sensation of falling from a height, 
with which a dream is usually associated. The sound may 
be distinctly heard if there is premature waking. 

I shall have presently to refer to the sounds that are re- 
ferred to the head, but I may anticipate this to mention a 
very curious instance of another sensation not quite auditory. 
If we conceive the function of the cochlea as blending into 
tone, by repetition, the quickly recurring waves that are 
rhythmical, it is a curious question how we should hear such 
musical notes if the cochlea were absent. If the waves had 
sufficient amplitude, sufficient impetus, and were not too 

* In passing I may note that if it is due to the stapediiis, which is supplied 
by the same nerve as the orbicularis palpebrarum, the facial nerv^e, thereMs 
this interest in it that the function of the stapedius is beheved to be to 
guard the labyrinthine structures from undue shock, by instantly contracting 
when sudden pressure tends to force in the membrane to which the stapes is 
attached, while the office of the orbicularis is, of course, to guard the eye. 
Thus each of these muscles which act together is the guardian of the organ 
of sense. 



APPARENT LOCALITY OF THE SOUND. 67 

frequent, they would be perceived as isolated sounds, as are 
the vibrations by the sense of touch. Indeed, a tuning-fork 
vibrating twenty times a second is thus perceived if held near 
the ear, the vibrations being too distant to be blended into 
a tone. A very intelligent woman, after the cessation, under 
treatment, of paroxysmal headaches, became liable to a musi- 
cal sound which seemed to fill the head and was accompanied 
with a strange feeling of extreme fulness of the head. Her 
hearing w^as perfect to all tests. She could hear Galton's 
whistle up to 16,000 vibrations a second. External noises 
prevented the subjective sound from being noticed. On 
sounding various tuning-forks she identified the sound as 
the middle C (between the treble and the bass). But 
the sound was always immediately preceded by a distinct 
sense of vibration in the head, which would sometimes re- 
main as such, and at other times change to the sound. When 
she touched the sounding tuning-fork with her finger she 
said the feeling was exactly the same as that of the vibration 
she experienced in the head. I give this curious fact without 
comment. I beheve the sensation was accurately described, 
and that the observation may be trusted. It is possible, per- 
haps probable, that the sensation was of central origin, but 
there must be a correspondence between the central action 
and peripheral excitation; sensations precisely such as are 
excited from the periphery may conceivably be of purely 
central origin. A similar sense of vibration is met with in 
other cases, although not frequently, and its associations de- 
serve careful study. A woman, aged 50 years, had laby- 
rinthine deafness, slight in the right ear, and moderate in the 
left, with slight continuous tinnitus, for many years. She had 
also had three attacks of more considerable tinnitus in the 
preceding four years, apparently in both ears, the second of 
which was said to have been accompanied with deafness, and 
yet with peculiar sensitiveness to sound, and to have ended 



68 SENSATIONS OF SOUND. 

soon after a great increase in the tinnitus. The last attack 
had existed for six months, and was characterised by a fre- 
quent sound in the head, either general, or more on one side 
or the other. It was usually a very rapid vibration, but at 
times had been like music, although not any definite tune. 
Yet if she heard a tune played on the piano she would often 
continue to hear it after the instrument had ceased. This 
case also illustrates the association of cephalic vibration with 
musical tone. It also illustrates the apparent co-operation of 
the centre in the effects of labyrinthine change. 

Reference to the Head. — These two cases are examples of 
the point next to be considered, the reference of subjective 
sounds to the head and not to the ear. The second case 
conforms to an explanation often given — that subjective 
sounds, produced simultaneously in both ears, seem to the 
sufferer to be in the head. This is occasionally true; but ex- 
ceptions are, I think, more frequent. Bilateral tinnitus may 
be referred solely to the ears, and sounds may be referred 
to the head which seem produced only on one side. We see 
in this, moreover, the difference between abnormal local ex- 
citation of the nerves and their normal stimulation; when the 
latter occurs on both sides the sound is always referred to an 
external cause. 

Sensations produced in one labyrinth are sometimes 
referred only to some one part of the head on that side. In 
one case of left-sided labyrinthine deafness, the sound 
Avas always referred to the left side of the head, but it 
seemed to spread when loud through the whole head ; it was 
never referred to the ear. In other cases I have met with, 
it has been referred to the parietal region, to the parietal and 
occipital, to the occipital only, and in one, with considerable 
nerve deafness, a persistent rumbling sound was always re- 
ferred to the region between the temple and the vertex, never 



APPARENT LOCALITY OF THE SOUND. 69 

to the ear or any other part. In these cases of one-sided 
head-sound the extension to the whole head, when the sound 
becomes louder, is very common. 

It is not easy to suggest an explanation of these varieties 
of locahsation. We may, however, remember that the sound 
of a tuning-fork, applied to any part of the head, is referred, 
approximately, to the region on which it is placed, quite 
apart from the sense of vibration communicated to the bone; 
although many or even most waves must reach the labyrinth 
by the membrana tympani and ossicles, they pass also from 
the bone to the membranous labyrinth, either directly, or 
through the perilymph. The correct localisation of the 
sound must be due to the precise group of nerve endings 
that are chiefly stimulated. Since the causes of labyrinthine 
tinnitus are for the most part random processes, the nerve 
endings may be affected in various combinations, and it must 
happen that sometimes these combinations are such as 
would be excited from some part of the skull. The same 
subjective localisation will then occur. The stimulation of 
the nerves of ordinary sensibility may help to guide the 
localizing discernment. Yet cases are met with which seem 
to baffle all attempts to explain the apparent localisation. A 
woman with slight bilateral nerve deafness, who was unable 
to hear high notes, and on the right side could not hear any 
tone above C^ (2 112 vibrations per second), described a con- 
tinuous squeaking sound, which was not referred to the ears, 
but seemed to her to be inside each parietal bone and to be 
louder on the side on which hearing was least affected. The 
subjective sound in this case corresponded nearly to that 
w^hich the patient was unable to hear — a noteworthy instance 
of the double effect of local disease in hindering and causing 
sensation. 

Localisation of Central Sounds. — It is a curious fact 



70 SENSATIONS OF SOUND. 

that the subjective sounds which originate in the auditory- 
centre in the cortex are referred to the same seats as those 
of labyrinthine origin. This is frequently the case with 
the central sounds included in this survey — those that 
occur as the warning of epileptic fits. When these are 
elaborate they are, it is true, referred to the external world, 
but when they are simple, or "crude," they generally seem 
to the patient to be produced either in the head, or in 
one or both ears. As examples I may mention a whistling 
sound referred to both ears, a similar sound referred to 
both sides of the head above the ears, a buzzing sound 
which seemed to pass through the head from one ear 
to the other, a whistle referred to the ear on the side on 
which the subsequent unilateral convulsion occurred, and a 
whistle seeming at the top of the head in one case and in 
another at the occiput. To the character of these epileptic 
sensations I shall have to return. 



CHARACTERS OF LABYRINTHINE SOUNDS. 

Some of the characters of the sounds that are due to 
labyrinthine disease have been already referred to, and others 
will have to be mentioned in connection with points yet to be 
considered. These variations are so great as to bafHe any 
attempt at minute classification, as they also baffie the 
capacity of language. Our vocabulary, however extensive, 
is quite inadequate to describe our sensations, and the similes 
to which the sufferer has recourse are often misleading. A 
rough division may be made into (i) crude sounds, such as 
hissing, humming, machinery, rumbling, and the like; (2) 
tones, as a whistle, a simple musical note, or the sound of a 
bell; and (3) elaborate sounds, such as music or voices, dis- 
tinct or indistinct. We cannot usefully separate the continu- 
ous and pulsating sounds, because a continuous sound so 



CHARACTER OF LABYRINTHINE SOUNDS. 71 

often becomes pulsating when it is louder, but the pulsating 
character is chiefly confined to sounds of the first class. It is 
probable that the difference is of significance when invariable 
— when a sound, for instance, remains continuous, however 
loud it at times becomes, or remains pulsating however slight 
it may often be. The precise character of sounds needs to 
be carefully noted, since it will probably prove to be impor- 
tant, when we obtain more careful and discriminating ob- 
sen^ations. 

Relation to Audition. — One feature which promises occa- 
sionally to be of definite practical importance, is the relation 
of the tinnitus to external sounds. In the majority of cases 
the subjective sounds are heard most when there is silence, 
sometimes are only then perceived. Doubtless external 
sounds often merely prevent notice, although we cannot be 
so sure that this is all. There are cases in which external 
sounds increase the tinnitus, and some of the facts are both 
curious and noteworthy. There may be a peculiar hypera- 
cusis, by which certain sounds seem especially loud and un- 
pleasant and increase the subjective sound. Although this 
feature suggests central co-operation the cases present e^d- 
dence of labyrinthine change. Yet such co-operation seems 
the only way to explain another symptom met with especially 
in this connection, the occurrence of an echo or repetition of 
the sound, not always in the same pitch. A man aged seventy 
years, with slight reduction of hearing, not equal on the two 
sides, experienced an echo with musical notes and high 
pitched voices; every syllable seemed repeated in a lower 
note, although of the same duration. I found that the sound 
of C^ tuning-fork and higher notes were thus repeated, but 
the middle C was not."^ It is difficult to explain the change of 

* The system of nomenclature of unusual notes employed in this lec- 
ture and the reasons for its adoption are fully explained in an appendix. 



72 SENSATIONS OF SOUND. 

pitch as of labyrinthine origin. But in one case of the kind 
the labyrinthine affection was secondary to disease of the 
middle ear two years before, with lasting perforation of the 
tympanic membrane. A rushing sound was varied by buzz- 
ing and by an occasional sound like the ringing of several 
bells. Loud sounds seemed to "pass straight to the middle 
of the head"; some notes of the piano were particularly dis- 
tressing, and the sound of these was repeated as an echo. 

Allied to this symptom is another — the addition of an 
abnormal quality to sounds that are heard. For instance a 
peculiar clanging character was added to all sounds in a 
gouty patient thirty-four years of age, who had labyrinthine 
deafness and also suffered from other forms of more simple 
tinnitus. This may be conceived as labyrinthine, but it is 
often associated with a sense of discord and with increased 
sensitiveness, hyperacusis, which may be either peripheral or 
central. It is often very difficult to say to which we should 
ascribe the origin of the sense of discord. All music sounded 
discordant to a woman aged thirty-seven, who had sHght 
double labyrinthine deafness, not equal, with simple tinnitus 
on the side of better hearing. On this she could hear the 
higher tuning forks (C^ and C^ and C, in the treble and 
below) better than the lower (C^ above the treble), but she 
could not hear any note of Galton's whistle. These symp- 
toms suggest that the discord was peripheral. But she also 
sometimes heard a sudden, spontaneous sound, as if some 
one had spoken to her, and the impression that this was 
a fact was strong for a moment, although she could never 
distinguish the words — a symptom which can hardly have 
been other than central. The production of a morbid 
functional state of the centre in consequence of the im- 
pulses that reach it, a state that involves the addition of 
sensations of central origin to those of labyrinthine source, 
is a question of some importance with regard to treatment. 



CHARACTER OF LABYRINTHINE SOUNDS. 73 

Simple hyperacusis is not common. In one case in 
which it was partial, but co-existed with slight deafness, the 
sounds which were perceived were heard too loudly. 
Again a highly cultured man, aged fifty-seven, had shght 
nerve deafness on both sides, with tinnitus chiefly on 
the left, seldom on the right. It was like "gas escaping," 
and he had an occasional noise in the head, described as a 
"churning." But a moderate sound was heard too loudly; 
water poured into a bath sounded to him like the noise of 
a waterfall, and the voice of a person speaking seemed not 
only unduly loud, but also confused, which made it difficult 
for him to distinguish the words, in spite of their loudness. 
It caused a distressing sense of mental strain, such as is met 
with sometimes in other cases. The strain seems due to the 
effort needed to perceive what is heard, suggestive of some 
degree of cerebral difficulty analogous to word-deafness. 

I may also mention the not uncommon cases in which all 
the senses are morbidly acute, in which, without sign of 
local disease, a combination of pulsating tinnitus and hyper- 
acusis is met with ; the arterial pulsations affect the nerves of 
the ear so as to influence consciousness. 

The threads of this subject interlace in such a manner 
that I have been led away from the special point — the in- 
duction of tinnitus by sound. It is not often well marked, 
especially in such tinnitus as can be reasonably regarded as 
labyrinthine; but the important point, in such cases is 
the beneficial influence of silence on them. A clergyman, 
aged 54, certainly gouty, began to suffer at the age 
of 50, from gradual deafness of the right ear, tinnitus, and 
attacks of vertigo. An aural surgeon found the meatus and 
middle ear to be normal. The deafness was almost complete 
to high notes, C^ (within the treble) being heard, but not 
C^ ; the voice, however, was heard fairly well. The subjective 
sound was continuous in character, but it was shght or absent 
7 



74 SENSATIONS OF SOUND. 

when there was external silence, and was excited by any loud 
sound of more than brief duration. A short ride in a cab 
would make it distressing, although at starting he was free. 
The effect of the music in his church was so great that for 
a time he had to abstain from duty, and the effect of his own 
voice, if he read aloud for an hour, was almost unendurable. 
Either influence would cause the sound to become such that 
he compared it to "the blowing off of a full head of steam 
in a locomotive." Even then, if he retired to his room, in 
perfect silence, the sound would gradually lessen, and in the 
course of two hours would cease entirely. In this case great 
benefit was obtained by following the indication thus afforded, 
and securing prolonged freedom from external sound. In 
another case of increase by external sounds, the tinnitus was 
also continuous, but there was no defect of hearing, even 
to high notes, only an inability to discern ''cross conversa- 
tion." 

Relation of Tinnitus and Vertigo. 

Many of the cases of aural tinnitus, which have furnished 
the ground for these remarks, were brought under observa- 
tion by the vertigo with which it is so frequently associated. 
But this common result of the irritation of the labyrinthine 
nerves is only within our survey so far as the subjective 
sounds are related to its occurrence. We refer the vertigo to 
the coincident affection of the semicircular canals by the 
same morbid process which, in the cochlea and vestibule, 
gives rise to the subjective sounds. That we are justified in 
doing so by the definite facts we possess is, I think, certain. 
The relation of the subjective sounds to the giddiness 
is, however, extremely variable. In current descriptions 
of aural vertigo it is often said that the noise becomes sud- 
denly and rapidly louder to a culmination with which sudden 
intense giddiness coincides. This relation is quite excep- 



RELATIONS OF TINNITUS AND VERTIGO. 75 

tional. Such increase of sound may occur and culminate, 
for instance, in a sudden crash, without any attendant giddi- 
ness. But a gradual increase often precedes the vertigo. In 
the case of the clergyman just mentioned the increased loud- 
ness of the sound was often followed by an attack of giddi- 
ness, until he learned the value of external silence. He 
found that when this had diminished the subjective sound he 
was safe from an attack of vertigo. This is a significant fact, 
although not one to be too hastily interpreted. It seems 
to show that there is a certain solidarity, so to speak, 
in the labyrinthine functions for which we should scarcely 
be prepared by the difference in their apparent character, 
although it agrees with the continuity of the labyrinthine 
structures. Moreover, we can trace a like solidarity in 
the corresponding central functions, as we shall presently see. 
In other cases the tinnitus exists only just before the vertigo, 
although without any increase or culmination. In a man 
aged 36, with labyrinthine deafness on one side only and 
attacks of severe vertigo, the sound occurred only for two or 
three minutes before each attack of giddiness. It seemed to 
him to be in both ears and was compared to a very loud 
roaring, without pulsation. But the sound may simply coin- 
cide with the giddiness and not precede it. This was the 
relation in several cases, with evidence of one-sided laby- 
rinthine change, causing deafness, in which the sound was 
pulsating and was compared to machinery, a steam-engine, 
and the like. In another case, of a clergyman aged 38, a con- 
tinuous hissing sound occurred only during attacks of giddi- 
ness, which were accompanied by nausea and sometimes by 
retching. The sound and the vertigo always began together 
and the sound ceased as the vertigo gradually passed away, 
in the course of a few hours. The sound was referred to the 
left ear, but no permanent deafness could be discovered; yet 
as long as the noise lasted, in spite of the fact that it was 



7j6 sensations OF SOUND. 

not very loud, he had great difi&culty in hearing ; a strong vol- 
untary effort was needed to enable him to discern the nature 
of external sounds. I have already mentioned this peculiar 
difficulty, needing a mental strain to overcome it, as probably 
a central symptom, and not rare. In some other cases 
with definite one-sided labyrinthine deafness, a pulsating 
sound, compared to machinery or a steam-engine, was also 
noticed only with vertigo. It is not easy to explain the sud- 
den paroxysmal effect of a process that is gradual and perhaps 
stationary. We have a similar phenomenon in the paroxys- 
mal hghtning pains of stationary tabes. These may occur 
during years, although the morbid process seems unchanged. 
These tabetic pains are perhaps a more pertinent analogy 
than the sudden attacks of pain in neuralgia, because we have 
good reason to refer the pains of tabes to the changes at the 
extremities of the sensory nerves, to which also our knowledge 
leads us to refer the attacks of tinnitus. Doubtless, causes 
which we sometimes can perceive, but more often fail to 
discern, determine the attacks, just as changes in the weather 
have so potent an influence in determining the pains of tabes. 



SOUNDS OF CENTR.\L ORIGIN. 

Let us leave the ear itself and turn to the centre to which 
its impulses pass. As I have said, in the symptoms of epi- 
lepsy we can feel reasonably sure that we have to deal solely 
with the features of central sounds, although we cannot hmit 
them to that disease. These higher auditory sensations vary 
very much in character; they may be crude or elaborate. I 
must pass by the subjective sensations which have a mental 
character, the auditory hallucinations and illusions, and those 
warnings of epilepsy which consist of a sense of spoken words. 
To touch upon their relations would carry us too far, and 
away from those with which we are specially concerned. 



SOUNDS OF CENTRAL ORIGIN. 77 

They have to do with instabiHty in the higher functional 
regions of the brain, as is illustrated by the fact that epileptics 
with such an aura are in far greater danger than others of 
becoming insane. The cruder auditory sensations which 
usher in a fit, severe or shght, deserve careful considera- 
tion. 

One curious fact is the occasional association of a subjective 
sound with a sensation of definite vertigo, which by itself 
is so common a warning. In some cases the central discharge 
mimics pure aural vertigo in a way that is alike curious and 
suggestive, as well as puzzhng. The difficulty that is caused 
in diagnosis is the greater because there are cases of aural 
vertigo in which the suddenness and severity of the dis- 
turbance produces actual loss of consciousness. These cases 
are quite distinct from epilepsy and yet the superficial resem- 
blance is close. This combined epileptic aura is another 
illustration of the fact of which I have just spoken — the very 
close connection which exists in the central processes between 
the two functions of the labyrinth, and also between the two 
symptoms which its disturbance generates. The sound 
which accompanies the epileptic vertigo is as simple as that 
which occurs in the labyrinthine form. The association is 
the more remarkable because all our knowledge points to the 
motor centres as the source of the sensation of giddiness, 
while that of sound is purely sensory. After all, however, the 
connection seems to illustrate and emphasise the fact I have 
already mentioned — the fact that, since all the sensory im- 
pulses produced at the periphery are perceived through a 
related activity of the higher centres, the functional processes 
in these must correspond to every peripheral process, and may 
present similar associations. 

Even the pulsatile character of aural tinnitus may be re- 
produced in the centre. It is unquestionably a rare symp- 
tom, but is of great interest. In a highly complex aura which 



78 SENSATIONS OF SOUND. 

I have recorded elsewhere,* a sensation of beating in the chest 
passed up to the head and there became a pulsating sound, 
accompanied by two lights before the eyes, w^hich approached 
with a rhythmical motion. We must, I think, ascribe this 
character to the mechanical influence of the arterial pulsations 
on the discharging centre. We know the influence of such 
pulsation upon pain; we know the susceptibility of nerve 
structures to mechanical influences, and we must assume that 
in the process of actual discharge, all their susceptibility is 
augmented. The influence is, therefore, not difficult to 
understand, w^hether the pulsatile pressure augments or hin- 
ders the progressive liberation of the nerve energy. It is not 
rare for the central sound to be described as "machinery," 
and this generally implies pulsation. But more rapid varia- 
tions may give the sensation the character of vibration, a 
feature we must attribute to the character of the nerve action 
itself. We have seen the relation of such rapid vibrations to 
low musical notes, and the nerve processes for this relation 
must have a corresponding development in the brain. A 
vibrating sound, compared to the noise of a faradic apparatus, 
was referred to the left ear by one patient as the warning of 
left-sided fits. Here, again, we have in a very curious degree 
the central reproductions of peripheral impressions, because 
such a sensation sometimes apparently originates in the ear 
itself. 

Although the elaborate sensations of psychical character, 
definite words and the like, are not within my subject, I 
may mention that in patients with such a warning of severe 
attacks, the minor attacks — petit mal — may be characterised 
by a quite simple auditory sensation. In one case of the kind 
simple "buzzing," referred to both ears, with obscuration of 
consciousness, constituted the sHght attacks, while the onset 

* In the preceding lecture on Subjective Visual Sensations. 



• CENTRAL CO-OPERATION. 79 

of the severe seizures was characterised by a vision of persons 
who seemed to speak inteUigible words. 



Central Co-operation in Labyrinthine Sounds. 

In leaving the higher centre we must, however, return 
once more to the labyrinth. A point that is not only of 
interest, but will prove, I think, of practical importance, is 
the co-operation of the centre in determining the character of 
the sounds produced by labyrinthine irritation. This is not 
difficult to understand when we consider how disturbing to 
the central structure must be constant abnormal impulses 
from the ear. The fact which raises this question is the fre- 
quency with which labyrinthine deafness is associated with 
sounds of such elaboration that it is very difficult to think 
that they are solely peripheral in nature. Another important 
question also is thus brought before us : What degree of elabo- 
ration of sound is consistent with a purely labyrinthine 
origin ? Of course, the crude, or simple, sounds, which have 
occupied us so much, we must regard as peripheral. On the 
other hand, elaborate sounds, such as a voice uttering distinct, 
or even indistinct, words, must be regarded as central. But 
there are other forms of tinnitus that cannot be referred with 
confidence to the labyrinth alone. To it, indeed, we may 
reasonably ascribe all sudden, simple tones, when we consider 
the analogy of the brief, momentary sensations of pain which 
are experienced in tabes, and the grounds we have for ascrib- 
ing them to the morbid action of the degenerated nerve end- 
ings. This apphes especially to the sudden sound of a bell, 
which is not rare, and even to repeated bell-hke sounds. But 
we must, I think, recognise a secondary central action in such 
a case as that of a woman, aged 43, in whom, after an attack 
of giddiness, bilateral tinnitus referred to the ears commenced 
and increased gradually. It was a buzzing sound, louder at 



8o SENSATIONS OF SOUND. • 

night. After a time there was an occasional change, for a 
few hours or days, to that which seemed to her just hke a 
band of musical instruments. She described it as so distinct 
that, although she could not recognise the tune, she believed 
that if she had been acquainted with harmony she could have 
written down the full musical score. At times also she 
seemed to hear voices, and, although she never could dis- 
tinguish words, the sound was that of a human voice, and 
occasionally she had seemed to hear herself called. But this 
was no hallucination. She referred all these sounds to the 
ears, and they never seemed to her, for a moment, to be of 
external origin. 

There is much more that I should like to say that I must 
leave unsaid. I should like to have referred to some con- 
ceptions of the process of stimulation of the special senses, 
which might estabhsh more unity in our thoughts, and with 
this to have considered the probable relation of the energy 
which excites the nerve impulse to that which is excited, and 
the nature of this. This subject is too wide for me to touch 
upon, but I would call attention to some other facts related 
to my special subject, although I can only mention them. 
One is the frequency with which labyrinthine tinnitus be- 
comes associated with unpleasant cephalic sensations, feel- 
ings of pressure, fulness, throbbing and the like, constant or 
varying, and sometimes related to the sound in a way which 
connects them with the tinnitus that is referred to the head 
itself. Another subject is the relation of tinnitus to paroxys- 
.mal neuralgic pain, either in the ear or head — a fact of much 
suggestiveness that well deserves study. But these at least 
for the present we must leave. 



PATHOLOGY OF TINNITUS. 8i 



PATHOLOGY OF TINNITUS. 

It is strange how few facts we have regarding the patho- 
logical changes which underlie the symptoms in the common 
class of cases, with deafness, tinnitus, and often vertigo, 
gradual in onset and often slowly progressive. It is strange, 
because our poor-law infirmaries and work-houses contain 
always many cases of the kind; it is strange, also, because 
modern methods have increased so much the reveahng power 
of the microscope, and because the present generation of 
workers are not prone to leave neglected any unexplored 
field. But \Ye can surmise much with reasonable sureness. 
In cases with striking and unusual symptoms, conspicuous 
changes have been found, concretions and the like. Further, 
we know that the parts chiefly concerned are of fibrous and 
epithehated structure, in which epithehal hairs receive the 
sound vibrations, which thus excite nerve impulses in the 
dehcate structures by which the two are united. We know, 
also, with what extreme readiness this process must be de- 
ranged and how^ minute a structural alteration may suffice. 
We know, also, that this membranous labyrinth may be the 
seat of acute inflammations, of which the most significant is 
that which occurs in early life, and sometimes in adults, as 
the effect of a peculiar blood state, often excited by cold, one 
of those toxic conditions Avhich have a special local incidence, 
for the inflammation is limited and symmetrical. It is now 
generally recognised that when there is complete deafness as 
the sole result of what was regarded as an attack of meningitis 
in early hfe, the malady was not meningitis but bilateral 
inflammation of the labyrinth, the general cerebral symptoms 
of w^hich may closely resemble those of meningitis. We have 
in this fact, not only the indication of a special blood state, 
but also of special susceptibihty on the part of the labyrinth. 
We know^ from many other facts that such susceptibility to 



82 SENSATIONS OF SOUND. 

acute inflammations of this kind on the part of fibrous struc- 
tures involves also a proneness to suffer from chronic changes 
in later life, especially in cases where there is an inherited 
rheumatic or gouty tendency, the tendency which may be 
called, and I think has been called, ''tissue gout." We can 
thus understand the fact, so often illustrated, that these 
chronic labyrinthine changes are especially common in such 
subjects. We also know that in late life, apart from such 
predisposition, the tendency to analogous affections of other 
fibrous structures is common. We see the great tendency to 
chronic rheumatism presented by the old, which we may 
ascribe to the influence on the tissues of waning vitality, 
coupled with the effect on the blood of the age-imperfection 
of the organs on which the blood state chiefly depends. It 
happens that only a week ago a pertinent illustration of this 
came under my notice. A man aged fifty-eight years, with 
some family history of rheumatism, although not of known 
gout, had suffered from vertigo and for some years from 
tinnitus and from deafness. His tissue tendencies were 
clearly shown by a contraction of the palmar fascia of one 
hand, on the ulnar side, passing down the little finger and 
keeping it flexed. The deafness was partly labyrinthine, 
but chiefly due to the middle ear, and the report of an aural 
surgeon (Mr. Field) on the cause of this was very instructive. 
He found considerable thickening of the membrana tympani 
on each side with complete fixation of the ossicles. The 
latter must be due to fibroid adhesions, while the state of the 
membrane was doubtless an indication of a similar change 
throughout the cavity, including no doubt the membranes 
which close the foramina leading to the labyrinth. Moreover, 
the clear evidence of labyrinthine deafness, in addition to the 
impaired conduction, leaves little doubt that there was a like 
condition in the labyrinth, although perhaps in a less degree. 
We cannot doubt the influence of such fibroid thickening on 



PATHOLOGY OF TINNITUS. 83 

the structure in which the epithehal hairs are connected with 
the nerve endings. Morbid processes of other nature, syphil- 
itic, traumatic, and the hke, are also met with in such cases. 

Primary Atrophy of the Auditory Nerve. — Very similar 
symptoms are, moreover, produced by a primary atrophy 
of the nerve, a subject to which I may briefly digress. I 
should like to utter an emphatic protest against the readi- 
ness to invoke atrophy of the auditor}^ nerve as the mor- 
bid state whenever labyrinthine deafness is recognised in 
conditions in which nerve degeneration is sometimes met 
with, and especially in tabes. It is, indeed, partly for this 
reason that I have preferred, for the most part, in this 
lecture, to use the term "labyrinthine deafness" rather 
than "nerve deafness." Statistics have been published 
in 'which in every case of tabes with any degree of laby- 
rinthine deafness, this impairment has been put down to 
atrophy of the auditor}^ nerve; such atrophy has therefore 
been said to exist in a considerable proportion of the cases, 
and the facts have been received and quoted as conclusive. 
Symptoms of more or less random labyrinthine changes, gen- 
erally non-progressive, are not rarely met wdth in tabes. The 
previous life of a large number of tabetic patients has been 
such as disposed them to tissue degenerations, and the effect 
of the blood state is often much increased by the diminished 
amount of exercise which the developed malady entails. 
Among all the cases — and I have careful notes of many hun- 
dred cases of tabes — I can count on my fingers those in which 
there was reasonable evidence of auditory nerve atrophy. 
Until, therefore, we have far more definite knowdedge of the 
symptoms of primary atrophy, more caution should be exer- 
cised in the diagnosis, or even suspicion, of this change. But 
we sometimes meet with evidence of the process which cannot 
admit of doubt. A man with tabes, who had bilateral deaf- 



84 SENSATIONS OF SOUND. 

ness, presented a progressive concentric limitation of the 
range of hearing quite similar to that which occurs so often 
in tabetic atrophy of the optic ner^'e. When first examined 
he was quite deaf on one side, and on the other could hear 
only the notes between G (within the bass) and E^ (above 
the treble), the range of audition being thus little more than 
two octaves. In the course of the next month the contraction 
of the range had reduced it to one octave, from middle E 
(on the lowest line of the treble) to E^ in the highest space, 
and so sharp was the limitation that while he could hear E 
he could not hear E flat, a semitone below; soon afterwards 
the deafness was total. But atrophy of the optic nerve does 
not always take the form of progressive concentric restriction, 
and it is not likely to be the only, and perhaps not the 
most common, manifestation of that of the auditory nerve. 
Atrophy of the optic nerve is so often progressive, when 
once established, that we are justified in regarding with sus- 
picion all cases of alleged auditory nerve atrophy in which a 
progressive course is not conspicuous. 

Functional State of the Receptive Structures. — It may 
seem strange at first that defective hearing should so con- 
stantly coincide with the production of these spontane- 
ous sensations. But the due reception of external stimuli 
and their adequate eft'ect upon the nerve endings must depend 
upon structural integrity, molecular integrity we may say, in 
the receptive elements. Organic changes in these may pre- 
vent the sound-waves producing their due efl'ect, and yet may 
also induce the molecular alterations in the terminations of 
the nerves on which spontaneous sensations depend. We 
may remember how frequently the distressing pains of tabes 
co-exist with loss of sensibility to pain, and also the dis- 
proportion between the effects on consciousness and the 
processes on which they depend, 



PATHOLOGY OF TINNITUS. 85 

Another fact of at least equal importance. In the normal 
condition all nerve structures must be in constant functional 
activity — at least, in some degree. This is necessary for the 
maintenance of nutrition; it is a necessary effect of vitality; 
it is essential for the capacity for full action on an adequate 
stimulation. In the case of a large number of nerves we are 
quite unconscious of this continuous functional activity. It 
need be only of the sKghtest degree, to subserve that constant 
renewal of molecules which must occur for life to be main- 
tained and function possible; but the phenomena of disease 
show us that a similar persistent action is also a part of the 
processes of life under abnormal conditions. It seems to be 
as constant when nerve endings have undergone shght de- 
generative changes as when they are normal. The morbid 
alterations in the fibrous tissue of the labyrinth, of which I 
have spoken, do not necessarily destroy the nerve endings, 
and they only interfere with their function in so far as the 
terminations are altered and the effect of sound-waves is hin- 
dered. We can thus understand that the subjective sounds 
are the result, under altered conditions, of the same vital state 
which normally maintains the nerve in perfect readiness for 
instant action.* We can understand that the damaged struc- 
ture, and altered molecular arrangements, while they do not 
impair spontaneous activity, change its form and increase the 
energy of the impulses. It is not, I think, difficult thus to 
perceive that the persistence of these sounds, which seem so 
strange, especially when combined with deafness, is due to 
one of the conditions on which the functional capacity of the 
nerve structures essentially depends. 

* Regarding this continuous activity see Professor Michael Foster's lec- 
ture in The Lancet of Nov. 7, 1896; also note by myself on "The Dual 
Activity of Nerve Cells," The Lancet, May 10, 1890. The words "nerve 
structure" should apparently be now used instead of nerve cells. 



86 SENSATIONS OF SOUND. 

TREATMENT. 

That which I can say regarding the treatment of these 
symptoms must of necessity be Hmited to general principles. 
Details I am obhged to omit, and if that which I say seems 
to be meagre, believe me this subject has been before my 
mind more definitely than any other. The treatment of these 
affections constitutes one of the most difficult and most ob- 
scure branches of therapeutics. This is not indeed surpris- 
ing. We have seen that to a large extent they depend upon 
chronic processes. Of all slow processes of disease it may be 
said that the morbid process, at every period and at every 
stage, is an accomplished fact. Damage and cicatrisation go 
hand in hand, but the process of cicatrisation is not recovery. 
In acute disease, the alterations caused in the tissue may pass 
away to a large extent, and the normal state to that extent 
may be reproduced. But a change indistinguishable from 
cicatrisation perpetuates all slow disease, and thus its effects 
necessarily endure. Still, even over these, we are not quite 
powerless, and we learn, on every side, lessons which should 
teach us to be slow to give up hope, or to relax our efforts to 
obtain that which we now lack. How impressive is the lesson 
we have just had from science that the w^ord "impossible" 
should find no place in our vocabulary. Even two years ago, 
had the wisest among us been asked the question: Is it pos- 
sible that before the end of the century we may be able 
to see through a deal door or a human leg — what would have 
been the answer? The humihty which this should teach 
should equally prevent us from limiting the possibilities of 
power in any department of our science or any branch of 
our art that is founded thereupon. The reason why, through 
this effort to discern some of the relations of those subjective 
sounds, their treatment has been ever before me, is because 
the first necessary step for the attainment of greater power 



TREATMENT. 87 

is more minute and accurate recognition of their features 
and relations. It is through these that we must hope to be 
able to apply, with more prospect of good, the measures which 
we already know to have some influence, and, by the dis- 
crimination they permit, to employ more wisely any means 
which the future may give us. Empirical measures, on which 
we are obliged so largely to depend in many other maladies, 
have at present almost no place in the treatment of tinnitus. 
We know, for instance, that the noises are sometimes lessened 
by bromide, although the influence of this is far less than on 
the vertigo which is so often associated. But we know 
also that the influence of bromide is especially exerted on the 
centres in the brain. I doubt, indeed, whether we have at 
present any evidence of its action on the peripheral nerve 
structures. But the evidence I have mentioned, that the 
auditory centres become secondarily involved in some cases, 
and give rise to some special features of the subjective sensa- 
tions, is reason for a careful systematic attempt to discern the 
relation between such central co-operation and the power of 
bromide to relieve the symptoms. The subsidence of the 
sounds in sflence, and the lasting relief thus afforded in 
suitable cases, I have already sufficiently dwelt on. There 
are many cases of labyrinthine tinnitus in which counter- 
irritation has a considerable influence for good, but there 
are also many cases in which it is powerless, and we are 
not yet able to distinguish the two. The distinction can 
only come, but probably will come, from careful discern- 
ment of the conditions under which the process develops 
and of the precise symptoms by which it is manifested. At 
present we cannot form any opinion regarding the significance 
of differences in the minute characters of the subjective 
sounds. We are already supplied with so many means of 
lessening the morbid action of other peripheral nerves that 
it will be strange if the future does not yield us means of 



88 SENSATIONS OF SOUND. 

lessening, at least in some degree, that of the nerves of the 
labyrinth. We can find little trustworthy guidance from 
experience of individual sufferers. In one labyrinthine 
case, it is true, the sound was always lessened by firm pres- 
sure on the posterior part of the temporal region, and the fact 
deserves to be remembered. Another patient found that a 
diminution was always caused by inclination of the head 
towards the side on which the tinnitus was heard, but this, 
I think, is only a special example of a more frequent influ- 
ence, — the sound may be often lessened by pressure on the 
arteries of the neck. Strange to say, this result has seemed to 
me more common when the tinnitus is a continuous sound 
than when it is pulsating.* I cannot now pursue the possible 
suggestiveness of this fact, but it leads up to another. I feel 
compelled to mention to you one case, which has been de- 
scribed in Germany,! on account of the importance of the les- 
son it conveys. An elderly man had gradually become com- 
pletely deaf in the right ear, with most troublesome tinnitus. 
The left ear was becoming deaf in the same way. The tinni- 
tus was so loud, so persistent, and so distressing that the man 
had several times declared that he could endure it no longer 
and must end his fife This proceeding on his part was made 
unnecessary by the treatment which was adopted. It was found 
that pressure on the carotid artery diminished the sound. 
The right internal carotid was therefore tied. It is very diffi- 
cult to understand the grounds for the operation. The blood 
supply to the labyrinth comes partly from the external carotid 
and partly from the basilar. The path by the auditory nerve 
to the opposite hemisphere is entirely within the blood supply 
of the basilar. The opposite auditory centre is supplied by 
the opposite middle cerebral artery. It is thus easy to under- 

* The fact of reduction of pulsating tinnitus by pressure on the vertebrals 
has been described by Dr. Dundas Grant. 

t Linsmayer, Wien. Med. Blatter, 1893, Nos. 8 and 9. 



TREATMENT. 89 

stand that the operation was found to have no effect whatever 
on the tinnitus. It produced left hemiplegia and left hemian- 
opia, and death resulted on the fifth day. I draw attention 
to this case because I think it should forever prevent the 
repetition of this operation for the rehef of labyrinthine tin- 
nitus. 

I must end this outline of some of the more prominent 
features of the subject, by reiterating the hope that it may 
at least serve to stimulate others to its careful study, and may 
serve to guide their observations. Provinces of medicine are 
often unproductive because they need more careful cultiva- 
tion than they have yet received. We have to till the fields 
to which our path may lead us, however barren they may 
seem to be, and hope that some of the seed sown, even upon 
stony ground, may germinate and bring forth fruit in time 
to come. 



NOTE. 



THE DESIGNATION OF MUSICAL NOTES IN SCIENCE AND 
MEDICINE. 

(" Review of Neurology and Psychiatry," April, 1903.) 

The convenient and accurate designation of musical notes 
has become a subject of importance to medicine and to science, 
especially to physiology. The system current among musicians 
has come down from the early days of the organ,* but it was 
adopted by Helmholtz and has therefore been used by most 
writers, since the pubhcation of his classical work on " Tonemp- 
findungen." But it is a system which has no rational foundation, 
except in organ construction, and with this it has only a partial 
connection. The absence of intelligible ground for it has had 
the necessary consequence of mistakes by those who have at- 
tempted to apply it to wider needs. It is not too much to say 
that error and confusion are met with as frequently as precision. 

The need for precise designation occurs in describing normal 
hearing, and still more in recording the hmitations of hearing 
met with in disease. The latter is as frequent in the work of 
the physician as in that of the aural surgeon. In the various 
senile and gouty changes in the internal ear, so often associated 
with vertigo, in the results of other forms of ear disease and 
central changes, and in the atrophy of the auditor}' ner\-e some- 
times met with in tabes, there is often pecuhar restriction of the 
range of audition. The method of designation by means of the 
number of vibrations per second is not convenient except for the 
higher notes, above the range of the tuning fork. For lower 

* It originated in the sixteenth centun', by a development of an earlier 
system, and was due to the extension of the notes of the organ. See Rock- 
stro's Art., "Tablature," Grove's "Diet, of Music." 

90 



DESIGNATION OF MUSICAL NOTES. 91 

notes the musician's method of designating the notes by letters 
and distinguishing by numbers the successive octaves is far better, 
and is generally employed. 

The term "octave" is in universal use as a name for each 
series of seven notes. It"" is apparently due to the fact that the 
eighth note is in unison with the first, although it really belongs 
to the next "octave." The more accurate term "septave" has 
been occasionally employed, first nearly a hundred years ago,* 
but few musicians have ever heard it. Since the series of musical 
notes, without added sharps or flats, has C for the keynote, 
the system of making each designated octave begin with C is 
universal. Each note of the series of seven being indicated by 
a letter, the successive series or "octaves" are distinguished by 
a number, or by strokes, after each letter, above for the higher, 
below for the lower. Instead of strokes or numbers, the method 
of doubhng or trebling the letters has also been employed. 

To distinguish the higher from the lower, some starting-place 
is necessary. The great source of confusion is that, in the current 
system (or what is supposed to be such), the starting-place for 
the higher and lower octaves is not a singly conveniently placed 
unnumbered octave, but is constituted by two octaves, both un- 
numbered, inconveniently placed, and distinguished by a differ- 
ence in the letters that indicate the notes. The upper one is in- 
dicated by small letters, the lower by capital letters. Each is 
unmarked, but the former is called the unmarked octave (the 
"unstroked," " ungestrichen " octave, because strokes were used 
of old instead of letters) ; the latter is distinguished as the great 
octave, apparently from some relation to the "great organ." 
The "unmarked" octave extends up from the C in the middle of 
the bass, the great octave from the C on the second leger-hne 
below the bass. 

This method will be better understood if the designations are 
added to the note-symbols as in the following table. It must 
be remembered that each octave extends upwards from the C to 

* In a rare little book on "The Art of Tuning," by Earl Stanhope, Lond., 
1806. A copy is in the Library of the Athenaeum Club, London. 



92 SENSATIONS OF SOUND. 

the B above. I have added to it a serial indication of some of 
the errors which are to be found in scientific and medical writings. 





Contra C. Great C. 


C tenor. C middle. C treble. C 


Cin 
in alt. 


Altmo. 


-1— 


/ 


m\' 


1 


• 1/ 


1 




\ 


1 


1 


^• 




L y\ 


m 










iri' 


• 




\ 1 1 










1 1 




VnL 


' 










C = 33 66 


132 


f^l 


-#- ' 


>6 2112 ■ 






264 528 10^ 


i224 


I. 

2. 

3- 
4- 


Contra. 

Helmholtz, . . Ci 
Tyndall, . . . Ci 
Bosanquet, . . C or ^C 
Banister, . . . C C 


Great. 

C 
C 
C 

c 


Un- 
mark- 
ed, 
c 
c 

CO 
C 


One Two 

time times 
mark- mark- 
ed, ed. 
ci or c' c- or c" 

Cl C" 

Ci C2 
c c 


Three Four 
times times 
mark- mark- 
ed, ed. 
c3 c* 
cm CIV 

C3 C* 
c c 


Five 
times 
mark- 
ed. 
c5 
cv 
C5 
c 


6^: 


Peterson, . . 
" Acoustics " 

Enc.Brit., . 
Foster, . . . Cj 
M'Kendrick, . Doi 


Ci 

C 
Doi 


C 

c 

Do2 


c c' 

C Cl 
Cl C2 
Do3 Do* 


c" 
Do5 


C3 
D06 


c"" 
Do7 




1. Helmholtz, "Tonempfindungen," dritte Ausgabe, 

2. "Lectures on Sound," quoting from Helmholtz. 


1870. 







3. Encyc. Brit., art. "Music," part ii. The capitals for the upper notes 

are about one quarter smaller than those for the lower. 

4. "Handbook of Music." The double C for C^ is open to mistake, 

although really clear. 

5. Art. "Harmony," Chambers's Encyc. 

6. Author's initials only given. The actual note adduced is A. "A3 is 

three octaves above the A between the second and third lines of the 
treble clef." 

7. Sir M. Foster's "Manual of Physiology," all editions. Only the upper 

and lower notes are given, but the series follows from the vibrations 
assigned to them. 

8. "Physiology of the Senses." "Fa" is the note given, but from the 

vibrations assigned to it in the several positions, the above series fol- 
lows with no unmarked octave. 
In Politzer's " Handbook of Diseases of the Ear," Eng. trans., Cassells, 
1883, the same note, C = 512, is referred to on page 167 as C^, 
and on page 178 as C. 



More examples might be adduced, but these suffice to show 
the confusion that has resulted under the present system of two 
unmarked octaves, in an arbitrary situation, for which no clear 
reason exists to help the memory or to induce uniformity. The 



DESIGNATION OF MUSICAL NOTES. 93 

distinction of capitals and small letters, the former for the few 
octaves below the C within the bass, and the latter for it and the 
numerous octaves above it, has evidently been felt by some writers 
to be an anomaly not worth conformity. This seems to have 
been the opinion of Grove, since in every article in his " Diction- 
ary of Music" similar capitals are employed for the high and low 
notes, wdth the distinction of some descriptive designation. 

It is not worth while to discuss in detail the examples of varia- 
tion I have given. Most are simple mistakes, as their examination 
will show. I have taken pains to ensure precision in every exam- 
ple. It is certain that in Science a more simple and a rational 
system is needed, if uniformity and exactness are to be secured. 
It seems also that in Music the need is scarcely less. There is 
no sharp division between Music and Acoustics, or between the 
latter and Physiology, 

For a useful system it is essential that there should be only 
one unmarked octave, or "neutral octave," as I think it might 
be conveniently termed. The best position for this is certainly 
the octave above the "unmarked octave" of Helmholtz and the 
Germans. This position is assumed in the article on " Acoustics " 
in the Encyc. Brit., and, for the higher unmarked octave, by 
Peterson ("Harmony") in Chambers's Encyclopaedia. Its ad- 
vantages have been strongly urged by Dr. Shinn, of the Guildhall 
School of Music, in a letter to the " Musical News," January 24th, 
1903, in the pages of which I had endeavoured to evoke some 
discussion of the subject. I first suggested that the higher of 
the two present "neutral octaves" would be most likely to obtain 
adoption, but the advantage of the octave above this is manifest. 
The neutral C is then that which is often fitly called the " middle 
C," between the bass and treble staves; C^ and C^ are each within 
the treble and bass staves respectively; C^ and Cg are each on 
the second leger-hne, below and above the respective bass and 
treble, and may be called the sub-bass and supra-treble. These 
words are a convenient and sufficient distinction in oral descrip- 
tion. It is not only desirable, but necessary, to secure precision 
and accuracy, that a consistent and reasonable method should be 
employed. 



94 SENSATIONS OF SOUND. 

The following will then be the method that is suggested: — 




38 66 132 264 528 1056 2112 4224 8448 16896 



Supra- 
Sub-bass Bass Middle Treble treble 



C, Ci 



C2 



C3 c* 



C5 



C6 



Tuning forks avail us up to C^, but the range of hearing ex- 
tends, in young persons, at least three octaves higher, and for 
these upper notes Galton's whistle is available. It is an instru- 
ment of the greatest service in the estimation of the function of 
the auditory nerve.* 

The symmetrv' of the suggested method will be more clearly 
perceived if the staves are placed vertically. 

Bass. Treble. 



c, c, c C^ c 

Moreover, the system aids the memory of the number of vibra- 
tions of these several notes. The bass C3 is 33 vibrations. The 
first (leger-Hne) C below the bass (C2) is the first with two figures 
(66), and the first above the treble (C^) is the first with four figures 
(1056), while the number of vibrations of C* (4224) is almost as 
easily remembered as C3. This may be a trifle, but it is a conve- 



* It is less known than it deserves to be. It is made by Hawksley, at the 
suggestion of Mr. Francis Galton. It may be well to mention to those who 
use it that it should be blown through from the mouth, not breathed through 
from the lungs, to prevent the interior of the fine steel tube becoming rusted. 
For the same reason it is well to draw air through the tube after use. 



DESIGNATION OF MUSICAL NOTES. 95 

nient trifle, and I have yet to learn that even that justification 
can be urged in favour of the old method, venerable as it is, and 
famiHar as it is to many. 

I may be permitted to end this note with one example of the 
need for uniform precision. In a book, published in 1885, I 
wrote this: "The patient is absolutely deaf to the loudest musical 
notes above E of the treble clef and below the lower G of the bass." 
The range of hearing afterwards lessened, "until only the notes 
between the two E's of the treble clef can be perceived." In a 
German translation"^ the passage is rendered: "fiir die lautesten 
musikahschen Noten liber E und unter contra-G volHg taub ist." 
. . . " Nur noch die zwischen E und E legenden Noten wahr- 
genommen werden." I may say that the G I intended to indicate 
was that on the lowest line of the bass clef, an octave above the 
"contra-G." 



* "Gehirnkrankheiten," von W. R. Gowers, ubersetz. von J.Mommsen, 
1886. 



LECTURE III. 

ABIOTROPHY; DISEASES FROM DEFECT OF 

LIFE. 

Delivered at the National Hospital for the Paralysed and Epileptic, Queen Square. 
Bloornsbury, on February 21, igo2.* 



Gentlemen: — Life presents to us a double aspect, and so 
therefore does death. One is its somatic character, the hfe 
of the organism as a whole, to which the words ''life" and 
"death" are chiefly applied. Somatic life depends essen- 
tially upon the blood, as familiar words assert, words uttered 
and written long centuries ago — "the blood which is the 
life thereof." It depends on the proper constitution of 
the blood, deficiency or perversion of which will end life 
speedily or slowly. It depends on the due reception of 
oxygen by the blood through the lungs. And it depends also, 
and most of all, on the due movement of the blood by the 
heart; if the heart is stilled, life ends almost instantly. But 
besides this general life, the termination of which involves 
that of every part of the body, many of these parts have their 
own vitality. Some of them may slowly die, while the life 
of all the rest goes on without impairment. They may die 
from many causes, some early, inevitably, from a grave defect 
of vital endurance; some much later, the failure being but 
slightly premature; and some at various times, apparently 
from various causes. When the failure is early it is often 
due purely to a defect in vitality, a defect which seems to be 



The Lancet, April 12, 1902. 
96 



DEFECT OF VITALITY. 97 

inherent, the tendency thereto inborn. We do not, indeed, 
apply the word "death" to this slow decay of the elements; 
we speak of it as "degeneration," but the process is in many 
cases, perhaps in most, an essential failure of vitaHty, and I 
think it is instructive to consider the degenerations in this 
aspect. But in doing so I am met by the difficulty, that we 
have no word by which to designate this conception — a de- 
generation or decay in consequence of a defect of vital endur- 
ance.* I do not like new words— indeed, I dislike them — but 
if we have a conception for which no name exists, which we 
need frequently to speak of, it is not wise, I think, to shrink 
from an attempt to give it a name. Here, the simplest mode 
of obtaining what we need is to insert the root of /5ro? after 
the negative particle in "atrophy"; this gives us "abio- 
trophy. " But it is generally better, if you can, to appropriate 
what you need than to make it afresh, and we find the word 
^iozpocpoc used in the sense of "vital nutrition."! If we 
prefix the negative particle we have the same word, "abio- 
trophy." If a more general term is desired, the adjective 
"biotic" has been occasionally used in Enghsh % in the sense 
of vital, and from this we may form "abiotic" to designate 
that which depends on defective vitality. A corresponding 
substantive would be "abiosis," and this also has some war- 



* This conception of the degenerations of the nervous system was admir- 
ably stated by Dr. F. W. Mott in his Croonian Lectures for 1900. But it 
formed the subject of an unpublished lecture which I gave in 1897 or 1898, 
and is epitomised, in its essential features, in some remarks which I made 
at a discussion on Tabes at a meeting of the Pathological Society of London, 
on December 5, 1899, reported in the Lancet of December 9 1899, p. 1591. 

t Not indeed in classical Greek: it is quoted by Stephanus from Gcrgias 
Pisides, a Byzantine writer of the seventh century (620 A. D.). 

t First in 1600. Dr. W. B. Carpenter added a .second adjectival termina- 
tion and made it "biotical." It exists in French as hiotique, from the Latin 
hioticus, and the Greek iSioTLnog, from fiiorog, and ajSiorog had the sense of 
"lifeless." Thus, "abiotic" is clearly legitimate. 
9 



98 ABIOTROPHY. 

rant. The word IScwfft^ was employed once or twice in old 
Greek, meaning "mode of life. " It is given us by the physi- 
cian, who is more widely known and esteemed, on account of 
the character and precision of his writings and the devotion 
of his life, than any other medical man who has lived — St. 
Luke. It is pleasant, I think, to take a word from him.* 
So I give you a choice of words by which to designate this 
unnamed conception. 



Cutaneous Abiotrophy. 

In most gatherings of men we may see an illustration of 
abiotrophy. We may perceive an illustration of the failure 
of the life of the hair folhcles of the scalp which must be the 
essential cause of early baldness. We are so familiar with 
the condition that we do not always perceiAT the lessons it 
may teach us. In many men most of the hair follicles die 
soon after adult life is reached — die beyond the power of 
restoration. Some, however, persist; around the circumfer- 
ence is a zone in which vitality is retained ; elsewhere the fail- 
ure is absolute and uniform. It is certainly often hereditary; 
father and son — indeed, also grandfather and grandson — may 
become bald between the ages of 20 and 30 years. Such 
decay is practically limited to the male sex. In other persons 
and families failure of vitality in the follicles occurs later 
and is less extensive. In others, again, a luxuriant growth 
of hair is retained throughout life. I know that baldness has 
lately been ascribed to seborrhoea, due to organisms, but such 
a cause, accidental and acquired, fails entirely to account for 
the more general features of the condition, and, if true, can 



* The word, previously used in the Septuagint, comes to us through the 
author of the Acts of the Apostles, but may have been used by St. Paul, since 
it occurs in his speech before Agrippa. 



CUTANEOUS ABIOTROPHY. 99 

be only an exciting cause, effective by reason of the failure 
in vitality.* 

Without complete degeneration of the follicles they may 
fail to produce the normal pigment of the hair, and early 
greyness is hardly less common than early baldness. It is 
not less instructive. It is a qualitative failure, an enduring 
defect of one function of the follicles. It shows that with- 
out the total failure of life part of the work of life may come 
to an end. That it must be by a chemical process that the 
pigment is produced I think none can doubt, and that hair 
may be blanched by a change in the follicular secretion is 
conclusively shown by the case of one-sided greyness of the 
hair of the head and beard produced in a few days by men- 
ingeal haemorrhage. f Regarding the association of greyness 
and baldness, not only may the imperfection to which grey- 
ness is due be extreme without any tendency to loss of hair, 
but it is said that baldness is seldom preceded by greyness. 
The persistent luxuriance of growth of the hair when the 
formation of pigment has ceased is a familiar fact. It is 
also worthy of note that even early greyness is met with in 
each sex, and does not present the tendency to affect males 
only, which is so conspicuous in premature loss of the hair. 



Muscular Abiotrophy. 

I must not be tempted to delay too long at the surface 
of the body, but we must not pass at once to the nervous 
system. Between the surface and the nerve centres we meet 
with tissues which present very striking and instructive forms 
of true abiotrophy — the muscles. In the various forms of 

* In curious contrast to the seborrhoeal theory is the conclusion of one 
German writer that early baldness is the result of the habit of daily washing 
the head. 

t Described in the following lecture on "Metallic Poisoning," p. 153. 

L.of C. 



loo ABIOTROPHY. 

idiopathic muscular atrophy, in which there is a primary 
atrophy of the muscular fibres, we have examples of a true 
abiosis. To all these primary myopathies it has become 
customary to apply the term "muscular dystrophy," and the 
custom is convenient, if not quite accurate. The term thus 
includes both simple muscular atrophy and its well-known 
congener, pseudo-hypertrophic paralysis. In these the mus- 
cular fibres, after full development, cease to maintain their 
nutrition. They slowly waste and a large number, most of 
them in many parts, all in some, ultimately perish. The con- 
nective tissue between them overgrows by a process we can 
discuss better in connection with the nervous system. Its 
increase may fail to maintain the normal bulk of the muscles, 
so that these waste conspicuously, sometimes extremely. In 
other cases this tissue-weed, as we may regard it, presents a 
more luxuriant development, and produces fat-bearing cells 
which so much increase the bulk of the muscle as to cause 
the enlargement of "pseudo-hypertrophy." 

These great variations in the interstitial process compel 
us to regard the failure of life in the muscular fibres as the 
essential element of the disease ; it is a defect of vital endur- 
ance, truly congenital in so far as the tendency is concerned. 
Two other facts indicate the same conclusion. The defect 
in the muscular system may not only be, as it were, qualita- 
tive, it may be also quantitative. Certain muscles may be 
absent, however early the sufferer is examined, especially 
the lower part of the pectoralis major and the latissimus dorsi, 
which depress the raised arm and are the least needed muscles 
of .the body, since gravitation will accomplish in most cir- 
cumstances that for which they are needed. We have further 
proof of its dependence on a congenital tendency in its occur- 
rence in several members of the same family and chiefly in 
the males, the girls, who do not suffer, conveying the morbid 
tendency to their own sons. Girls, indeed, may suffer, but 



RELATION TO SEX. loi 

less frequently in affected families than in the isolated cases 
which we sometimes meet with. Remember that all heredi- 
tary and family diseases sometimes arise de novo. I shall 
have to return to the point again, for it is important. 

We saw the special tendency of males to suffer from bald- 
ness, we shall see the tendency also in the affections of the 
nervous system; its manifestation in pseudo-hypertrophic 
paralysis is striking — even more so, I think, than in simple 
idiopathic atrophy. You may have heard of the group of 
cases through which Dr. Meryon first made the disease 
known in this country. Four boys, all the sons in one family, 
died from it; the girls were unaffected. But I know that 
one of these has two sons, and both are affected in an extreme 
degree. Her daughters are quite well. I could give you 
other examples which have come under my own observation 
which are equally marked, but the fact is too well known 
to need further illustration. I will only remind you, before 
passing from these muscular maladies, of the unequal way in 
which the muscles suffer. The distribution of the affection 
is strikingly different from that of those atrophies which de- 
pend upon the nervous system, but its locahsation varies also 
in the different varieties of muscular dystrophy we are able 
to distinguish. 



Abiotrophy in the Nervous System. 

Let us pass to the degenerations of the nervous system. 
In all those with which we are concerned to-day there is a 
slow decay of the nerve elements which have a common 
function — a decay limited to these but extending through 
their entire extent. Our modern conceptions lead us to 
regard these functional tracts as nutritional entities and to 
term them neurons. Each depends for vitahty on the cell 
from which the fibres proceed — a chief process ending in a 



I02 ABIOTROPHY. 

long fibre, and short processes quickly branching in the spongy 
grey matter. We have long recognised this relation to the 
cell, but the change in our conception has come, as you know, 
from the perception of discontinuity. The division of the 
fibres (which is really the separation of their constituent 
fibrillar) terminates in ultimate branches which seem to end, 
but they end in contiguity to others from which they are 
stimulated. The groups of neurons which are differentiated 
in function, differ also in their tendency to decay — in their 
degree of vitality. When decay occurs slowly, it seems to be 
the result of a slow failure of the influence of the cell on which 
their vitality depends, and indications of degeneration are 
first seen in the parts that are furthest from the cell — in the 
extremities of the fibres. But these neurons differ not only 
in the lapse of life, but also in its early stage. Not only do 
they die at different times, but they vary in the time of their 
development. Some are structurally complete sooner than 
others, and thus are distinguishable in the beginning of life 
as well as in its ending. 



Interstitial Overgrowth. 

Before we consider the special forms of the slow failure 
of these neurons, the forms of neuronic abiotrophy, there is 
another feature of the process of decay which it is important 
to discern. Whenever the nerve elements waste there is 
always an overgrowth of the interstitial neuroglia, the con- 
necting and supporting tissue which lies between them. This 
overgrowth may be, indeed, on first inspection, the most con- 
spicuous element, and its aspect has led the process to be 
termed "sclerosis." I say "its aspect," because there is 
generally no increase of consistence in the part so changed. 
This is generally diminished; the interstitial tissue, which 
looks so fibrous and firm under the microscope, is really softer 



INTERSTITIAL OVERGROWTH. 103 

than the nerve elements that have perished. This over- 
growth has certain features which it is important to recognise. 
They have much significance in connection with conditions 
which we shall presently consider. The neurogha is a resi- 
due of the embryonal tissue from which the nerve elements 
also develop. When there is local arrest of development of 
the latter, as in cases of congenital fissures and cavities in the 
spinal cord, this embryonal tissue persists in tracts adjacent. 
The two elements, the neural and neuroglial, seem to have 
a common but inverse vitality; it is in consequence of this 
that the interstitial tissue overgrows when the nerve elements 
decay. The overgrowth seems to coincide with the very 
commencement of the decay, and may be at first the more 
conspicuous. When it is thus started it often proceeds with 
an independent energy; in consequence of this, it may soon 
become much more obtrusive, and may overstep the strict 
limits of the degeneration and pass a little into adjacent 
tracts. It is especially luxuriant where the connective tissue 
is naturally most abundant, about the vessels and at the 
surface of the spinal cord, beneath the pia mater. On account 
of this the nature of the process was for a long time misun- 
derstood. The significance of the extent of the degeneration, 
through the whole of a single tract of nerve fibres, did not 
receive its due weight as an indication that the degeneration 
of the nerve elements was the primary process. Attention 
was fixed upon the more conspicuous interstitial tissue, and 
the characters of this were thought to be evidence that it 
was the primary change and that it started from the vessels 
or from the membrane. The word "sclerosis" itself made 
the mistake easier, because there are some morbid processes 
in which this element is primary, as in disseminated sclerosis. 
For these reasons the degeneration of the motor tract in the 
lateral columns of the cord is still spoken of as "lateral 
sclerosis," and degeneration of the fibres in the posterior col- 



I04 ABIOTROPHY. 

umns is called "posterior sclerosis." I may add that we 
have another illustration of the tendency to independent 
growth of this tissue in the fact that the residual tracts which 
persist when the development of the cord is arrested, may 
take on a new process of growth at some period, usually in 
early adult life, so as to give rise to that which seems a definite 
new formation, the condition termed "gliomatosis. " 

Not only is the secondary overgrowth thus excessive in 
degree, but it sometimes assumes an energy which entails 
some vascular disturbance, as active tissue-growth is always 
apt to do. This may even be such as to constitute a process 
of an inflammatory character and it seems, even in rare cases, 
to be attended by haemorrhage. At least there is occasionally 
a rapid or even sudden increase in the symptoms, not other- 
wise to be explained. Let me give you an instance. The 
optic nerve is a structure in which the amount of interstitial 
tissue which is formed in primary degeneration is exception- 
ally large. It is so in the simple atrophy of tabes. In this 
we sometimes have evidence that the interference with func- 
tion is especially great at the optic commissure, so as to cause 
temporal hemianopia, an indication that focal damage is 
added to the primary atrophy. We can understand this if 
the secondary change assumes at the commissure an inflam- 
matory degree. This is also indicated by the fact that such 
temporal hemianopia may develop rapidly. I have seen one 
case, and another has been recorded, in which, when such 
hemianopia had developed, it progressed to complete loss in 
one eye and then the remaining half field was suddenly lost, 
causing complete bhndness, as if the vascular disturbance of 
the secondary process had led to a haemorrhage at its chief 
seat. We also sometimes meet with evidence that axial retro- 
ocular neuritis, an interstitial process, develops in the course 
of simple atrophy, a fact which has the same significance. 
We shall presently see the importance of these considerations. 



SPECIAL FORMS. 105 



Special Forms. 



Let us pass to the special forms of degeneration of the 
nervous system which seem to be abiotic. We may distin- 
guish certain groups, to which I referred at the outset. The 
first consists of those in which the failure of vitahty occurs 
before, or soon after adult hfe is attained, and it may be 
quite early, soon after structural development is complete. 
In many cases of this group the relation to an innate tendency 
is shown by their occurrence in several members of the same 
farnily, in brothers or sisters, and sometimes in more than 
one generation. But each form, even those in which a 
family grouping is most marked, may occur in isolation. 

The natural transition from the muscular to the nervous 
system is by the fibres which end upon the muscles, the 
spinal motor neuron, whose vital centre is the cell of the 
anterior grey matter of the spinal cord. Note this: different 
as they are in aspect, of all structures the muscular fibres 
are nearest to the nerves. The muscular fibre is excited to 
instant contraction by the stimulus that reaches the extremity 
of the nerve fibre, which ends in contiguity to the muscle 
protoplasm, although the two are not continuous. So also 
the nerve impulse which stimulates the muscle arises, we now 
conceive, in the extremities of the branching processes of the 
cell, as the result of an impulse that reaches the ends of 
other fibres which are contiguous but not continuous. Re- 
member, also, that the life of the muscle depends upon that 
of the nerve. The muscular tissue has indeed its own vitality, 
which may fade, as we have seen, independently; but it has 
a mysterious dependence on the nerves. Slow atrophy of the 
muscle follows the slow degeneration of the nerve. The 
atrophy might be thought to be due only to disuse, were it 
not for the change in electrical excitabihty which so soon 
presents itself — the "reaction of degeneration." But if the 



io6 ABIOTROPHY. 

degeneration of the nerve is of rapid, and not only of rapid, 
but of irritative character, the muscular fibres undergo a 
similar change, a more irritative degeneration, a quick de- 
struction, with granular and fatty degeneration and a rapid 
disappearance of all electrical excitability. These facts indi- 
cate a close vital relation between the muscular and nervous 
structures — a relation we may call one of functional vitality, 
as distinguished from inherent vitality. 

Of the many forms of abiotrophy in the nervous system, 
perhaps the most striking is one of which these spinal motor 
neurons are the seat. It is rare but it has been observed 
many times.* It commences soon after they have attained 
structural completion, about the end of the first year of life, 
and progresses so rapidly as to cause almost universal paral- 
ysis and death at the end of the fifth or sixth year. It occurs 
in families as well as in isolated cases, and also in both sexes, 
and thus must be ascribed to a congenital defect of vital 
endurance. After death there is found almost complete 
degeneration of the motor cells of the spinal cord, with very 
little change in the white columns, degeneration of the 
anterior roots and of the motor fibres down to the muscles, 
and extreme degeneration of these. It has, indeed, been con- 
jectured that both the motor neurons and the muscles suffer 
simultaneously; whether it is so or not we cannot say, for 
the affection of the motor neurons is sufficient to account 
for the muscular changes. It is quite certain that the de- 
generation of the motor nerves is not a consequence of the 
muscular atrophy. In extreme idiopathic muscular atrophy 
the nerves may be unaffected. A striking proof of this is 
afforded by a case which was observed by Duchenne and 



* See especially Hoffmann, "Deutsche Zeitschrift fiir Nervenheilkunde," 
Band i8, 1900; Ibid., vol. xx. Cramer, " Centralblatt fiir Allegemeine Pathol- 
ogic," 1895. Senator, "Charite-Annalen," xxvi. "Jahrgang," &c. 



SPECIAL FORMS. 107 

published by him when the patient was nine years old ; it was 
afterwards observed and described when the patient was 28 
years old by Landouzy and Dejerine. The patient died when 
she was 36 years old, but the thorough pathological examina- 
tion that was made has only lately been published.* In spite 
of extreme degeneration of a large number of muscles of hmbs, 
trunk, face, and neck, the motor-nerves and spinal motor- 
cells were absolutely normal. 

But the abiotic infantile atrophy presents one remarkable 
feature; the affection begins in the muscles of the hip and 
thigh and trunk, and thence extends, reaching last the ex- 
tremities of the limbs, which suffer first in the ordinary form 
of spinal atrophy. This is a feature presented both by muscu- 
lar abiotrophy and by this remarkable neuronic form. Such 
common features are noteworthy as links between the mus- 
cular and nervous systems. A similar form of neuronic 
atrophy is occasionally met with in later childhood and early 
adult life. . In some forms the cerebral motor neuron also 
suffers, the upper segment of the motor tract, as it does in 
the atrophies of later life. The isolated decay of this cerebral 
motor neuron is also met with in early adult life as an abiotic 
degeneration of the lateral columns — the pyramidal tracts. 
It is manifested by spastic paraplegia, coming on often with- 
out any exciting influence and sometimes in several members 
of the same family. f Occasionally the malady has followed 
some influence, such as an acute disease, which would depress 
the nutritional vigour of the whole nervous system, but has 
an enduring effect only on structures whose vitality is defec- 
tive, and might soon fail without this influence. 

* Spiller, Cont. Pepper Labor., Philadelphia, 1900. 

t See, for instance, the cases recorded by Dr. Howard H. Tooth, "St. 
Bartholomew's Hospital Reports," vol. xxv.; Strumpell, " Neurologisches 
Centralblatt," 1901, p. 628; Krafft-Ebing, "Deutsche Zeitschrift fiir Neurol- 
ogic," 1900; and Finzi, "Rivista Sper. di Fren.," xxi. 



io8 ABIOTROPHY. 

I have here to show you an example of such abiotic spastic 
paraplegia. It is the more instructive because it is isolated; 
such sporadic cases are far from rare. Their nature is often 
not discerned, because it is not suggested as it is when other 
members of the family suffer. The patient is 20 years of age, 
and his symptoms commenced gradually about three years 
ago without any cause to which they can be attributed. 
There is no suspicion of inherited or acquired specific disease. 
He has weakness of the legs, with some spasm, excessive knee- 
jerk and foot-clonus, with no change in sensibility, and no 
girdle pain. He has also some unsteadiness, suggestive of 
some failure in the posterior columns. The abiotic nature of 
the case is confirmed by the fact that another system of 
fibres is also faihng. He has atrophy of the optic nerves 
which also has developed gradually and presents the aspect 
of simple atrophy. The simultaneous occurrence of such 
degeneration in two neuronic systems at this period of hfe 
leaves no doubt of its nature. 



Optic Abiotrophy. 

The optic nerves frequently suffer from abiotic wasting. 
Many groups of cases are on record in which several members 
of the same family have become blind, usually between the 
ages of 15 and 25 years, from a slow failure of the nerve fibres, 
progressive in spite of treatment. A full account of these 
cases has been given by Dr. S. H. Habershon.* This pro- 
gressive course places their essential nature beyond doubt; 
yet it is obscured by the fact that the early stage has very 
often been accompanied by symptoms of retro-ocular neuritis, 
even with slight signs of it in the disc. There has often been 

* "Transactions of the Ophthalmological Society of the United King- 
dom," 1888, p. 190, where references to the chief ^ATitings on the subject will 
be found. 



OPTIC ABIOTROPHY. 109 

a central scotoma indicative of an "axial neuritis." The 
change, moreover, has often been preceded by a cause capable 
of inducing such neuritis, especially tobacco-smoking, or in 
the case of women some acute disease. We may understand 
this fact better, I think, if we remember what I said just now 
regarding the independent energy of the interstitial over- 
growth that concurs with degeneration of the nerve elements. 
We may also remember the great amount of interstitial tissue 
that is formed in the optic nerves, even in primary tabetic 
atrophy. Tobacco amblyopia is apparently due to an axial 
neuritis, which gradually ceases, and its effects pass away 
when the cause ceases to act. But the loss of sight, in the 
cases I am now speaking of, goes on steadily increasing after 
tobacco has been given up. It goes on as by a progressive 
atrophy of the nerve elements, without any increase of the 
signs of neuritis, showing that the toxic agent was only the 
exciting cause of the process really due to an inherent defect of 
vitaHty. In those who are not smokers the toxine of an acute 
disease seems sometimes also to act as an excitant. We know 
that the toxine of scarlet fever may cause pronounced optic 
neuritis. The difficulty is to understand that optic abiotro- 
phy, wasting of the nerve-fibres from defect of vital endur- 
ance, should apparently begin by interstitial inflammation. 
But let me remind you of what I have just said regarding 
the interstitial overgrowth which attends the atrophy of the 
nerve elements. Secondary as it seems, it may be simply 
simultaneous. There seems to be a sohdarity in the nutri- 
tional energy of the two tissue elements, the neural and 
neuroghal, and the tendency to overgrowth of the latter 
may be synchronous with the tendency of the life of the 
former to cease. The tendencies are in the opposite direc- 
tion, but they seem to be coincident results of the same vital 
condition. If so, we can understand that the tendency of the 
interstitial tissue may cause it to respond with readiness and 



ii6 ABIOTROPHY. 

energy to a toxic influence which can act upon it, and that 
thus retro-ocular neuritis, the effect of a toxic agent, may 
concur with the very commencement of the abiotic wasting 
of the nerve elements, and that its special symptoms may even 
seem to lead the way. It is not a little curious that in the 
patient before you, with abiotic spastic paraplegia and optic 
atrophy, we find indications of the same associated process 
that I have described. As far as its course and the ophthal- 




Fig. 14. — Fields of \'ision. The upper fields are for white; the lower repre- 
sent the central region, the field for red (continuous fine) and green 
(broken line). In the upper fig\ires the outer line is the normal field. 



moscopic appearances are concerned it seems to be a primary 
simple atrophy of the optic nerve. His acuity of vision is 
reduced to one-tenth. The fields present a peripheral re- 
striction, but no central defect in the fields for white can be 
detected, even with a small object. Yet it is different with 
the colour fields. There is a well-marked central scotoma 
for both red and green (see accompanying chart). It is 



FRIEDREICH'S DISEASE. iii 

irregular in outline, but extends to an average of about io° 
from the fixing-point, and in one eye to 20°. This, of course, 
suggests axial neuritis, and led to an inquiry regarding 
tobacco-smoking; we learned that he had been accustomed 
to smoke as much as half an ounce of shag tobacco a day! 
Thus this agrees with other cases of optic abiotrophy which 
I have mentioned in presenting shght symptoms of axial 
neuritis and in the fact of the same exciting cause. But it 
presents the progressive tendency and also the peripheral 
restriction of the field and the aspect of disc met Avith in 
ordinary atrophy, while its abiotic nature is indicated also 
by the coincident affection of the cerebro-spinal motor 
neurons. 

Friedreich's Disease. 

The spinal symptoms in this patient, the spastic palsy and 
unsteadiness, due to atrophy of the motor neurons and those 
which conduct to the cerebellum, are such as often form part 
of the best known abiotrophy, Friedreich's disease, the so- 
called "hereditar}^ ataxy." The latter name is another in- 
stance of inaccurate terminology, because the evidence of 
heredity is not so common as is the affection of collaterals, 
of brothers and sisters. This "family" feature is clear proof 
of the congenital nature of the tendency to vital failure which 
the disease manifests. Friedreich's disease is really ataxic 
paraplegia, depending upon slow changes in the posterior 
and lateral columns, but associated with other symptoms in 
speech, etc., and in it the abiotic tendency is clearly congen- 
ital. Males suffer more frequently than do females, but not 
in the same degree as in some other analogous maladies. 

Friedreich's disease was the first of the kind to be distin- 
guished and is the best known, but observation has revealed 
the wide variation in the precise characters presented by 
cases which cannot well be separated from typical forms. 



112 ABIOTROPHY. 

The characteristic symptoms, the weakness and unsteadiness 
of the legs, sometimes ataxy of the arms, the change in speech, 
and the nystagmus, are often found to be associated with 
some impairment of sensation, and with either loss or excess 
of the knee-jerk; the condition of speech also is found to vary, 
and there may or may not be mental alteration. The cases 
pass by degrees into another group which has been thought 
to be distinct. In this the most conspicuous feature is the 
swaying disturbance of equilibrium when standing, with or 
without evident weakness of the legs; there may be loss or 
excess of the knee-jerk, but there is seldom any disturbance of 
cutaneous sensibility. The arms may present any form of 
incoordination or none. Speech is commonly altered, slow 
and monotonous, sometimes with confluent articulation, 
sometimes with a staccato utterance. There is almost always 
nystagmus, and mental change is more often marked than in 
Friedreich's disease. The difference in other symptoms is 
generally one of degree only and depends on the age at which 
symptoms come on. This is chiefly during the second half 
of actual childhood. Resemblance of the symptoms to those 
of disease of the cerebellum has caused the malady to be 
called by the inexact and clumsy name ''heredo-cerebellar 
ataxy. " Although heredity has been found in a few cases, 
merely a family association has been commonly met with. 
Disease in the lateral columns has been found, but the changes 
are greatest in the posterior columns and the direct cerebellar 
tract, which seem to convey afferent impulses to the cerebel- 
lum; their defect deranges its coordination of impulses that 
guide the cerebral motor centres. Damage to these upbear- 
ing fibres, conveying impressions from the muscles, seems thus 
to cause this peculiar "cerebellar" ataxy, as distinguished 
from the pure incoordination of the legs met with when the 
inbearing fibres to the cord degenerate, as in ordinary tabes. 
All the facts regarding the disease show that it is a true abi- 



LATER NEURAL ABIOTROPHY. 113 

otrophy, a degeneration of certain neurons from defect of 
vital power, but the precise distribution of the defect varies 
in different cases. Probably many of the neurons in the 
brain which connect different parts, which associate and har- 
monise their functions, also waste, and thus the mental change 
may be explained. But the special pathology of this affection 
is beyond my present subject. 

Before I leave this group of abiotrophies, those of earlier 
life, it may be well to point out that not all the morbid states 
which seem congenital are really such. Caution is especially 
needful in the case of the diplegias which date from birth, 
because they are so frequently due to meningeal haemorrhage 
during a tedious or instrumental labour. The narrow pelvis, 
which causes this in one child, may have the same effect on 
another, and thus we may have the semblance of a family 
affection in that which is purely acquired. The birth dam- 
age tends to improve as time goes on ; abiotrophies tend to in- 
crease, although when shght in degree they seem sometimes 
to become stationary. The varying course observed in both 
muscular and nerve affections makes it probable that the 
degree and extent of the deficient vital endurance may vary 
much in different cases, with corresponding variations in the 
tendency of the symptoms that it causes. 



Later Neural i\BiOTROPHY. 

The second group of degenerations are those which occur 
at the other end of hfe. While general vitahty still seems 
full of vigour, the nutrition of some neurons fails ; they slowly 
die. The neurons which most frequently thus decay are the 
spinal motor neurons — those which sometimes fail, as we have 
seen, at the very beginning of hfe. According to the position 
of the tracts which suffer first and most, the effect is the symp- 
toms of spinal progressive muscular atrophy or of labio- 



114 ABIOTROPHY. 

glossal paralysis. These are more frequent in late life than 
isolated degeneration of the upper motor neuron which causes 
spastic paralysis, although this sometimes suffers alone, and 
almost always degenerates when the lower neuron suffers. 
These maladies often come on without any apparent cause, 
simply because the term of life for those structures is reached 
sooner than for the vital organs; they decay in a true abio- 
trophy. When any exciting cause can be traced it is usually 
one which is inadequate alone — some general depressing in- 
fluence, such as anxiety or grief, which must act equally on 
all the other structures and tissues, reducing the vital energy 
of all. But vitality only fails in those which have inherently 
a less degree ; their defect is sufficient to make the reduction in 
these, though the same as in the others, relatively greater in 
effect, sufficient to end their life. Without this influence they 
might or might not have persisted to the end of general life. 
The apparent cause does not lessen the significance of the 
facts which show that these affections are essentially senile 
abiotrophy. 

Mental change, especially simple mental failure, often 
occurs under the same conditions, and no doubt from a slow 
degeneration of cerebral neurons which connect and combine 
others in a way we cannot yet perceive. Another senile 
malady, paralysis agitans, must be referred to vital failure in 
some cerebral motor structures. In its conditions and course, 
it is a striking example of a cerebral abiotrophy. In spite 
of its obvious seat in motor structures, in spite of its strongly 
progressive character, it seems never to entail the decay of the 
motor neurons which connect the brain, the spinal cord, and 
the muscles. It formerly seemed to me like a degeneration 
peculiar in kind, such as we are reminded of by that which 
causes the hair to become white from lack of pigment though 
growth is still luxuriant, which presents a contrast to the de- 
generation which causes baldness. But the recent discov- 



TOXIC AND TOXINIC DEGENERATIONS. 115 

eries compel us to look to the extremities of the branching 
processes of the motor cells, the dendrites which pass into 
the spongy grey substance, for the source of the motor im- 
pulses which are conducted by the fibrils that pass through 
the nerve-cells without interruption. A change in the nutri- 
tion of the dendrites may disorder function, yet leave un- 
affected the vital cell and the nutrition of the neuron as a 
whole. It is also conceivable that there may be a change 
in the relation of the dendrite endings to those which stimu- 
late them and induce the motor impulses. We know too 
little to be able to form an adequate hypothesis. But the 
conditions under which paralysis agitans generally occurs 
and its course show that it must be regarded as the expres- 
sion of a special defect in vitality — as a form of abiosis. Its 
occasional occurrence, even in extreme form, in middle life, 
also without discernible cause, is consistent with this view, 
for the same is true of other senile maladies. 



Toxic and Toxinic Degenerations. 

A third group of degenerations remains, large and impor- 
tant. They are the varied degenerations that occur, especially 
in middle life, as the result of some definite cause. It is not 
clear how far these are due to a defect of life. The degenera- 
tion may be the result of the presence in the blood of some 
material which is able to enter into the constitution of the 
nerve elements, but is not adequate for their proper func- 
tional or structural maintenance. They may slowly recover 
if the supply of the noxious matter ceases. Arsenical neuritis 
is an example. Arsenic seems capable of taking the place of 
phosphorus in metabolic changes of nutrition, but its pres- 
ence deranges function and also structure, so that degenera- 
tive change is the result. The alteration begins where vitality 
is weakest, at the extremities of the nerves furthest from the 



ii6 ABIOTROPHY. 

nutritional centre, the cell; the energy of this may ultimately 
be impaired, but we have not evidence that the primary in- 
fluence is exerted on the cell or that the process consists 
essentially in a failure of vital energy — that it is a true abi- 
otrophy. The same statements may be made with regard to 
alcoholic neuritis, since the process in this has the same 
features. 

The most common neuronic degeneration of the middle 
period of life is tabes. This, as you know, must be ascribed 
to the influence of a post-syphihtic toxin. But it occurs so 
long after the primary disease and at such a variable interval 
of years, that the question arises — Is the affection of the 
nerve elements due to the constant presence of the toxin in 
the system, in varying quantity and varying degree of toxic 
power, or has a transient toxin an influence in reducing future 
vital endurance? In the latter case it may be regarded as 
acquired abiotrophy. Each hypothesis has difficulties, but 
neither is quite inconceivable. On the whole, I think the 
first is that which best explains the facts of the disease. The 
analogous toxin of which we know most — that which causes 
diphtheritic paralysis — has been proved by Sidney Martin to 
be due to a change in the chemical constitution of albu- 
minoses, caused by a ferment-like material which the organ- 
isms in the throat produce. The toxin varies in its character, 
to judge by its different effects, and it is noteworthy that it 
may sometimes act on the same neurons as are affected in 
locomotor ataxy and give rise to the same symptoms. It is 
conceivable that such a change in the chemical constitution 
of albuminous substances, once set up, may continue, and the 
toxin may be constantly produced, in varying amount and 
varying toxic power, its formation being modified from time 
to time by other influences of which we know nothing. In 
the processes concerned in the production of excess of sugar, 
we have an example of the persistence of the derangement of 



TOXIC AND TOXINIC DEGENERATIONS. 117 

a chemical process, and the gradual increase of the derange- 
ment if not restrained, and although the analogy is not very 
close (since sugar is a normal constituent of the blood) it 
illustrates that such disordered chemistry may be enduring. 
The occasional rapid increase in the symptoms of tabes, such 
as may bring a patient from a stationary slight degree to the 
most extreme disabihty in a few days, is better explained 
by the sudden production of a poison of greater amount or 
power, than by the sudden reduction of the resistance of 
structures the vitality of which is impaired. The same con- 
clusion seems suggested by the great improvement which we 
meet with in some cases. A man came in here about two 
years ago who had had, for some years, symptoms of the first 
stage of tabes, and then in the course of a few days the ataxy 
increased to such a degree that he was not able to stand, 
from the extreme incoordination. Retention of urine had 
developed and cystitis had set up a suppurative orchitis. Yet 
this patient gradually improved until he could walk without 
much unsteadiness before he left the hospital, and now he 
can walk well for eight or nine miles. Unfortunately, im- 
provement does not always occur in such cases of rapid exacer- 
bation. There is one tabetic process the course of w^hich is 
more uniformly progressive, so much so, indeed, as to re- 
semble closely the effect of reduced vitality — the atrophy of 
the optic nerves. But even in this we meet with cases which 
become arrested, usually as the result of treatment. The 
significance of this fact we cannot discern or even wisely 
speculate about. 

Arrest or improvement from treatment occurs in other 
slow degenerations which occur during the middle period 
of life; some of them are met with occasionally as the 
sequelae of syphilis, but they may occur without obvious 
cause or as the result of exposure to cold, or they may seem 
to be due to the toxin of some other specific disease. The 



ii8 ABIOTROPHY. 

nature of these also is doubtful. Some of the progressive 
muscular atrophies of middle life resemble the senile form 
we have just considered in their slow commencement and 
gradual extension and increase, and often in the absence 
of a cause. Yet they differ in being more amenable to treat- 
ment. There is a considerable prospect that such cases will 
be permanently arrested. But even in such cases after 
syphilis, it is not by anti-syphilitic treatment that good is done, 
but by the hypodermic injection of strychnia. In one typical 
case the malady commenced just after a course of treatment 
at Aix, but the permanence of the arrest induced by strychnia 
is shown by the fact that it has now been absolute for about 
twelve years. In another case, more advanced but also 
arrested, the treatment was commenced after a rapid increase 
which occurred during the administration of iodide of potas- 
sium. This treatment has not the same influence in the 
senile abiotrophic form. 

That terrible malady, general paralysis of the insane, 
seems, often at least, to be due to the same cause as tabes, 
symptoms of which are so often associated, and seems to 
be of the same degenerative nature, produced no doubt in a 
like way. That which has been said of tabes applies to it 
also, and that which has been said of the interstitial altera- 
tions, and their independent energy, may explain the inflam- 
matory changes often met with. But here we are on uncer- 
tain ground. The pathological relation of the morbid process 
to its cause is quite obscure. 

Just as the simple baldness which develops in early man- 
hood may also come on at any period in adult life and in 
any degree, so the family abiotrophies which usually com- 
mence early in adult hf e or in childhood may show themselves 
later. In the families in which some members suffer early, 
in other members the same symptoms may occur only during 
middle life — a fact which we can understand by the concep- 



CONCLUSION. 119 

tion that the degree of vital energy in such cases is greater, 
the vital endurance is such as to persist longer. Yet the 
occurrence of both early and late forms in the same family 
shows that their nature is the same and that the difference is 
one of degree. 

Conclusion. 

These conceptions I hope may help you, if not to under- 
stand these processes, at least to think of them more clearly, 
I would especially impress upon you the fact which is illus- 
trated by the lad whom I have shown you — the sporadic 
occurrence of these abiotrophic diseases. Their nature is 
easily discerned when they occur in groups which have the 
tie of consanguinity, but the discernment is less easy when 
the diseases occur in isolated form. Remember the signifi- 
cance in such cases of the age of the patient, the slow develop- 
ment of the malady, the absence of adequate cause, whether 
an inadequate cause can or cannot be traced, and the corre- 
spondence of the symptoms to the functions of certain sets of 
neurons. Many cases of this kind are regarded as due to 
disseminated insular sclerosis, often assumed to exist when 
the symptoms afford no justification for the opinion and in 
cases in which the assumption is disproved by the future 
course of the disease. Remember that the symptoms of 
systemic degeneration are not alone ground for the diag- 
nosis of insular sclerosis, nor is the additional presence of 
nystagmus. Nystagmus on movement of the eyes is met 
with in many spinal degenerations of pure systemic type, 
why we do not know, but the fact deprives it of the diagnostic 
importance which has often been attached to it. 

My object in this lecture has been to present to you the 
fact that many degenerative diseases of the nervous system 
are a result of a defect in vitaHty. The two aspects of death 
which I mentioned at the outset are very different in our 



I20 ABIOTROPHY. 

practical view. Somatic death is that against which we ever 
strive, which we endeavor to postpone as long as may be. 
The other form of death — the termination of life of isolated 
structures in the body — is to us what we call disease. It 
does not of necessity involve the termination of general life, 
but it is not less to be striven against, although the strife 
must often be in vain. The discernment of these diseases, 
which we may call "abiotic," and the recognition of the 
symptoms, the course, and the conditions which indicate 
them, is of extreme importance. Their discernment may 
save you from many errors and may prevent many mistakes, 
both in your forecast and your treatment. We must en- 
deavour to check their progress, for we seldom know the 
strength or feebleness of the tendency, or whether it can or 
cannot be hindered, but the perception of the nature of these 
maladies will often help you. It will enable you better to 
perceive why treatment fails, and it may save from useless 
prolongation of attempts to gain that which cannot be, and 
it may sometimes save from waste of money that can ill be 
spared, and from the waste of hope which means only 
deeper disappointment. 



LECTURE IV. 

MYOPATHY AND A DISTAL FORM. 

Delivered at the National Hospital for the Paralysed and Epileptic. 



Gentlemen: — In the last lecture I gave here, I considered 
the various maladies that depend on defective vitality, on the 
imperfect vital endurance of the tissues which causes their 
nutrition to fail, generally early in life, sometimes later. I 
suggested that this decay, which results from defect of life, 
might be called "abiotrophy," and the word has been wel- 
comed as convenient and useful. I illustrated the condition, 
as some of you may remember, by the wasting of the hair 
follicles of the skin which causes premature baldness, by the 
forms of muscular dystrophy which often occur in families, 
and have thus their essential vital nature strongly empha- 
sized, and also by the many forms of degeneration in the 
nervous system that are of the same nature, which vary 
according to the special structure that fails, the time of life 
at which the vital failure begins, and the cause which some- 
times seems to be its incidental excitant. 

I have to return to the same subject to-day in one of its 
special manifestations. We are all opportunists, more or 
less, and I am able to show you some examples of muscular 
abiotrophy which are so instructive as to compel me to take 
them as my subject to-day. You know that these primary 
affections of the muscles are called "idiopathic muscular 
atrophy," "myopathy," and also "muscular dystrophy." 

* British Medical Journal, July 12, 1902. 
II 121 



122 MYOPATHY AND A DISTAL FORM. 

The last name (due to Erb) means "difi&cult nutrition," and 
has a certain aptness, because there is often an overgrowth 
of the interstitial tissue which suggests the idea of a struggle 
for existence, such as we sometimes see between weeds and 
the proper crop which has been sown on the ground. The 
metaphor is not quite precise, nevertheless we shall see that 
it is not without a deeper justification. In the form which 
is termed " pseudo-hypertrophic paralysis," of which I am 
fortunately able to show you two instructive cases, this inter- 
stitial growth attains a special luxuriance. Fat cells are 
formed in the fibrous tissue that develops, and from this 
there is an enlargement of some muscles, whence has come 
the common name of the disease. It was given by Du- 
chenne, who had been specially struck by this feature, the 
more so because it had chanced to him to meet with some 
cases in which the enlargement attained a rare extension and 
degree, being present in most of the muscles. He used to 
claim Raphael's child-angels as examples of the disease. 
Some of you may remember the extraordinary development 
of their muscles depicted in the celebrated cartoons. In 
the early days of this Hospital there hung, over the fireplace 
in the consulting-room, an engraving of Raphael's picture, 
"The Transfiguration"; in it is shown a child with de- 
moniacal possession; it was placed there as an appropriate 
representation of an epileptic fit, or the most accurate known 
in art. On a visit Duchenne once paid to the Hospital, I 
remember that he pointed out the figure as one which might 
well pass for an example of the disease on which he had 
bestowed the name. 

But there may be no increase in size of the muscles, or 
there may be a decrease. The interstitial tissue may merely 
compensate for the wasting of the muscular fibres or it may 
fail to do so. Hence, in the same case, we meet with muscles 
that are weak and large, that are weak and normal in size, 



INTERSTITIAL GROWTH. 123 

and that are weak and small. Interstitial growth, which is 
luxuriant, or moderate, or slight, is seen in the same case; 
one or the other may preponderate in different cases. Names 
are often instructive, but they sometimes obscure. I think 
that Duchenne's designation hindered the recognition of the 
fact which has been established by Erb and others that 
neither the amount of interstitial tissue, nor its character, 
is an essential element of the disease. The constant element 
is the change in the muscular fibres themselves; some of 
them may appear at first unduly large, but many are small 
and present the features of degeneration; ultimately this be- 
comes general, irrespective of the increase of the interstitial 
tissue. It is a true abiotrophy. 

As to these differences, let me remind you of what I said 
in the last lecture regarding the growth of interstitial tissue 
which occurs in the nervous system when there is primary 
atrophy of the nerve elements. I pointed out the variation 
it presents, and that it sometimes attains a luxuriance and 
energy which make it overstep the strict limits of the degen- 
erated tracts. This feature at one time raised a suspicion 
that it was the primary element in the process, and a similar 
suspicion regarding the muscles was excited at first by the 
abundant development of interstitial tissue, especially in 
the pseudo-hypertrophic form. Let me remind you also of 
another fact I pointed out. When we consider the features 
of this double process, the atrophy of the functional struc- 
tures, and the overgrowth of the interstitial tissue, they sug- 
gest that the two elements have a vital relation, common in 
the necessary connection of the life of each, but opposite in 
tendency. When the nutrition of the muscular or nerve 
fibres begins to fail, that of the interstitial tissue is increased. 
It does not grow merely to fill up space; it is not truly a 
secondary process, it is the expression of an excess of vitality 
simultaneous with the diminution of that in the proper 



124 MYOPATHY AND A DISTAL FORM. 

structures. The two tendencies, plus and minus, seem to 
be synchronous in these cases of vital failure, and the excess 
may have results at first more conspicuous than the dimi- 
nution. The interstitial growth may be at first much more 
obtrusive than the atrophy of the functional elements. We 
saw how, in the optic nerve, it seems to promote the response 
of the interstitial tissue to the influence of a toxic agent 
(tobacco) in the form of interstitial neuritis, the symptoms 
of which lead the way, but at an earlier age than the toxic 
influence alone is effective. Aloreover, when this influence 
ceases to act, the usual improvement does not occur — the 
abiotrophy still goes on. The same initial excess of vitality 
of the connective tissue seems to induce the exuberant de- 
velopment of the interstitial tissue in the muscles, and the 
production of fat cells within it, in muscular abiotrophy. 

The degree of overgrowth varies in degree in different 
parts and also in different cases, from causes we cannot dis- 
cern, yet we can understand its features better if we remem- 
ber the double character of the process. But the excess of 
the interstitial vitality is only temporary. It often attains 
a conspicuous degree before the failure of the life of the 
muscular fibres is considerable, but afterwards, as their 
failure becomes great, the vital energy of the interstitial 
tissue fails also. It is an initial outburst of energy; ulti- 
mately it also shares the vital failure. The fat becomes 
absorbed, and the fibrous tissue gradually contracts, so that 
the muscles, at first large, lessen but become more firm, and 
those which are not enlarged shrink; ultimately almost all 
become small as they become more and more feeble, only 
some trace of enlargement may linger long where it was at 
first so great. 

We shall see these states in the patients I have to show 
you. They determine variations in the aspect of cases in 
which the same muscles suft'er in dift'erent ways, and still 



PSEUDO-HYPERTROPHIC FORM. 125 

greater variations are due, as we shall see, to the difference 
in the distribution of the aft'ection. Under the microscope 
are some sections which are worth your inspection. One is 
from the deltoid muscle of a case of pseudo-hypertrophic 
paralysis, and in it you can see the excess of fibrous tissue 
and the fat cells between the muscular fibres, and that many 
of these are narrowed and others are undergoing structural 
degeneration. Under another is a section of the lumbar 
enlargement of the spinal cord of the same case; in this you 
mil see that the grey matter and nerve cells present a normal 
aspect, although the condition of the legs was one of almost 
complete loss of power. Under the third microscope I have 
placed a section of much interest as well as rarity. The part 
of the section under the microscope looks precisely hke a 
section of muscle in pseudo-hypertrophy. Narrow striated 
muscular fibres course among tissue composed mainly of 
fat cells with some strands of connective tissue. But it is a 
section of a small tumour attached to the spinal cord — a 
myolipoma. It had caused no symptoms, and was discov- 
ered by accident, at least if the phrase can be apphed to that 
which is revealed by a careful search, without definite object. 
But it is instructive, because it is evidently a fragment of the 
embryonal tissue of muscle which is developed in a wrong 
place, and in a wrong way. It shows how morbid develop- 
ment results in the condition we find in this disease, and 
illustrates its truly '^abiotrophic" nature. 



Pseudo-hypertrophic Form. 

I cannot, for lack of time, and I hope I need not, describe 
the general symptoms of pseudo-hypertrophic paralysis, but 
I may point out some symptoms that are illustrated by the 
cases I have here. The first is a boy of seven, who is still in 
the early stage. His case seems alone in his family. I in- 



126 MYOPATHY AND A DISTAL FORM. 

sisted in the last lecture on the fact that all family maladies are 
prone to occur in isolated form, and how important it is to 
learn to recognize them by their characters and course, be- 
cause so often you have not the evidence of their nature 
afforded by other cases in the same family. 

In this child no muscles are sufficiently increased in size 
to attract much attention, but the calves are distinctly large 
and firm. The knee-jerks are slight, but are not lost, as they 
are in the later stage of the disease. He is just acquiring the 
characteristic method of getting up from the floor, aiding the 
extension of the knees by putting his hands on them. This 
transfers some of the weight of the trunk from the upper end 
of the femur to its lower end, from the place at which the 
power exerted by the rectus acts to least advantage, to the 
place near the fulcrum at which the advantage is greatest. 
You may ask if this action is due to the weakness of the 
extensor of the knee, why is it characteristic of this dis- 
ease, since these muscles are often weak from other causes ? 
The question is a reasonable one. The action is not abso- 
lutely characteristic ; it is met with in other maladies, but in 
such it is very rare. This particular method of aiding the 
defective movement seems to be acquired only when the 
weakness comes on slowly during the development of mus- 
cular abihty. As a matter of fact it is so rare under other 
conditions that its diagnostic importance is very great. 

The boy presents two other symptoms, the significance of 
which I was, I think, the first to point out.* One is that the 
infraspinati are enlarged quite as conspicuously as the calf 
muscles. When the muscle is put in action, as you can see, 
it appears as a rounded prominence. The other fact is the 
atrophy of the latissimus dorsi and lower part of the pecto- 



* " Pseudo-hypertrophic Muscular Paralysis." London: Churchil 
1879. 



PSEUDO-HYPERTROPHIC FORM. 127 

ralis major. These sometimes are absent, and often, as here, 
are reduced to small dimensions. Their loss is often so 
great, even at an early stage, as to suggest a congenital de- 
fect. 

The disease is far advanced in the second boy I show you. 
His weakness became conspicuous at the age of seven, and 
he is now fourteen. He lost the power of standing four years 
ago, about a month after an attack of scarlet fever. The 
acute disease seemed to induce a rapid increase in the symp- 
toms; you should note this, because the symptoms of abiotic 
failure often first attract attention after some acute disease, 
such as scarlet fever or influenza; and the malady is ascribed 
to this influence, although it really existed before. It is easy 
to understand that an aft'ection commencing gradually may 
have been unnoticed, and that a depressing influence, which 
really only accelerates, may seem to be the cause. In this 
boy the calves are not absolutely large, but they are so in 
comparison with the other muscles, which are extensively 
wasted, and are weak even out of proportion to the wasting. 
He has hardly any power of flexing the ankle or extending 
the knee or hip, but these movements are also prevented by 
the great contraction which has supervened in the opponents. 
Permanent shortening occurs very readily in this disease 
from contraction in the interstitial tissue. When the power 
of standing has been lost, such shortening quickly fixes 
the limbs in the position naturally assumed in the sitting 
posture. In this child the contraction of the calves is great, 
and that of the flexors of the knees and hips is such as to 
prevent extension beyond a right angle. The calf muscles 
contract earliest and most, doubtless on account of the 
amount of interstitial tissue in them. The tahpes equinus 
that results, often prevents the patient from standing and 
walking, long before the weakness of the other muscles w^ould 
do so. Once the muscles lose the nutritional influence of 



128 MYOPATHY AND A DISTAL FORM. 

use, they rapidly become weaker, and this weakness, once 
estabhshed, is irremediable. We shall presently see the 
practical importance of this. 

We can still perceive some enlargement of the infraspinati, 
although less than in the former case; the characteristic 
atrophy of the latissimus dorsi and lower part of pectoralis is 
present in an extreme degree. But of all the muscles of his 
body, that which is enlarged in greatest degree is the lower 
part of each serratus magnus. You can see how these mus- 
cles stand out when he endeavours to push his arms forward. 
I have seen it before, and indeed it is shown in a figure in my 
"Manual," but it is not common. The influences which 
determine the character of the morbid process in the different 
muscles are quite unknown to us. 

His arms present characteristic weakness, least in the fore- 
arms and hands. The muscles of the neck are so feeble that 
he has some difficulty in holding up his head. The clavicular 
part of each sterno-mastoid is hardly to be detected, and this 
is a noteworthy feature, common to many forms of myop- 
athy.* The muscles of the face have here fair power for the 
most part, but the closure of the eyehds is feeble, and the left 
orbicularis is much weaker than the right. This is impor- 
tant; the difference between the two sides emphasizes the 
morbid character of the weakness. I may add that the elec- 
trical excitabihty of the muscles is lessened in both of these 
patients in proportion to the wasting, equally to each cur- 
rent; this is the characteristic condition in these diseases. 
In this patient the knee-jerks can no longer be obtained. 
Their gradual disappearance is an almost constant feature. 



* I noted this feature as long ago as 1879. (" Pseudo-hypertrophic Par- 
alysis.") 



FACIO-SCAPULAR FORM. 129 



Facio-scapular Form. 



The weakness of the orbicularis palpebrarum, which I 
have just pointed out, is of interest as another of the 
many links which connect the various forms of muscular 
dystrophy. It is especially great in a variety in which the 
face is affected in extreme degree, and so are the muscles 
of the shoulder and upper arm and trunk. As a rule, in 
this form, wasting accompanies the progressive weakness 
without conspicuous enlargement. From the distribution 
it has been called the " f acio-scapulo-humeral type," and 
also, from those w^ho called special attention to it, it has been 
designated the "type of Landouzy-Dejerine." 

I show you now a striking example of this form, and his 
aspect is strangely similar to that of a patient of whom figures 
are given in my "Manual." * I could fancy this w^as the same 
patient a few years older. I am able to show him to you by 
the kindness of my colleague, Dr. Beevor, under whose care 
the patient is. I must leave it to him to demonstrate the 
special features, but I would ask you to note the extreme 
weakness of the orbiculares palpebrarum. It is so great 
that the patient cannot completely close the eyelids. Com- 
mon as is the palpebral weakness, in few diseases of this 
class does it attain the degree seen in this form of myopathy. 
Yet a characteristic case of myasthenia has lately come under 
my notice in which the eyelids cannot be brought together by 
any effort — another link between myasthenia and myopathy. f 

Extreme as is the weakness of many of the muscles in this 
facio-scapular form, great as is the ultimate degree of their 
atrophy, however long its duration, the malady seems to be 
purely muscular; the nervous system, even the motor nerves, 



* Vol. I, third ed., Figs. 169-171. 

t British Medical Journal, May 24, 1902 



I30 MYOPATHY AND A DISTAL FORM. 

are unchanged. The fact rests on many observations, on no 
one more striking than that which has been recently pub- 
hshed by Spiller of a case described in the early seventies by 
Duchenne himself, in which life only terminated at thirty- 
eight.* We might wonder that disuse did not involve 
structural change in the course of so many years; but we 
must remember that the inabihty of the muscular tissue to 
respond to the motor impulse does not mean that the motor 
impulses themselves are less than normal. This question, 
however, would lead me far from my present subject. 



Distal Myopathy. 

The last case I have to show is one to which I would 
specially direct your attention because it presents unusual 
features. Indeed, I have not seen a similar case, nor do I 
know that one has been recorded, but it is always improbable 
that any given morbid state has not been seen before, and has 
not been described somewhere in the vast expanse of medical 
literature. 

This boy is eighteen years of age, and is the eldest of three ; 
the others are healthy. No similar case can be heard of in his 
family. The symptoms first attracted notice when he was 
ten or twelve years old; then it was noticed that he often 
caught his toes against the ground in walking. At a later 
date his hands were found to be weak. This feebleness of 
hands and feet has slowly, steadily increased, until now it is 
great. He is quite unable to flex the ankles, although he can 
just extend the toes, and can move each foot shghtly in and 
out by the tibialis anticus and the peronei. He can extend 
the ankle-joint by the calf muscles with some force. The 
movements of the knee and hip are performed with good 

* Proc. Pepper Lab., Philadelphia, 1900. 



DISTAL MYOPATHY. 



131 



power; the knee-jerks are present, but the left is less than 
the right. The thigh muscles are of normal size; the ante- 
rior tibial muscles are distinctly smaller on the left side; the 
calves, on the other hand, are rather large, and are firm. 
They are sufficiently large to suggest a resemblance to the 
condition in pseudo-hypertrophic paralysis, and they may 
have been larger in the past, for his mother spontaneously 
told me that their size had often attracted attention. 

Similar weakness is present in the upper limbs. His grasp 
is extremely feeble. With the right hand he cannot move 
the dynamometer, and with the left he can only move the 
index to 2 K°, instead of 50 or 60, as he should. Extension 
is also feeble; he can get the fingers, with the wrist, into line 
with the forearm, but cannot fully extend them when the 
wrist is over-extended. This is a convenient index of slight 
deficiency of power in these muscles. The muscles of the 
forearms and hands are small, but present no wasting com- 
parable to that which we see in progressive spinal atrophy. 
Above the forearm, the muscles have fair power and present 
no wasting; only a trifling atrophy of the middle part of the 
trapezii can be observed. In the affected muscles electrical 
excitability is lowered in proportion to their feebleness, and 
equally to faradism and voltaism. 

But this is not all. His neck muscles are normal, with one 
noteworthy exception — the sterno-mastoids. Of these only 
a trace remains — only a small fasciculus of the sternal part 
can be put in action by the will or electricity. The clavicular 
part seems quite absent. The condition is of such a char- 
acter, and is so similar on the two sides, as to suggest rather 
a congenital defect than an actual atrophy. It is a feature 
connecting the condition with other myopathies. We have 
just seen a similar deficiency in pseudo-hypertrophic paral- 
ysis. The platysma here seems also absent. 

The condition of his face is noteworthy. The movement 



132 MYOPATHY AND A DISTAL FORM. 

of the lips seems unimpaired. His tongue, however, pre- 
sents a curious aspect of wasting on each side, yet it moves 
properly, and there is no impairment of the palate. His 
smile, especially on the right side, presents too little move- 
ment outside the corner of the mouth "in proportion to the 
elevation of the upper lip. But the most important weak- 
ness is in the upper part of the face. He cannot raise the 
eyebrows at all; the frontales are powerless. Closure of the 
eyes by the orbiculares is also weaker than normal; their 
contraction is easily overcome, and more easily on the left 
side than on the right, conclusive evidence that it is morbid. 
This weakness of the orbiculares is met with, as I have said, 
in many forms of myopathy ; it is thus of considerable signifi- 
cance, and so are the weakness of the frontales, and the 
atrophy of the sterno-mastoids. All these features stamp 
this case as a primary myopathy, and yet it differs from all 
recognized forms in the purely distal distribution of the affec- 
tion in the limbs, and the normal state of the muscles near 
the trunk. In other forms the preponderant weakness and 
wasting are in the muscles moving the proximal parts, of 
the shoulder girdle and the hip, of the elbow and the knee. 
In the upper limb this is very conspicuous. In the leg the 
affection of the calf muscles is usually attended with weak- 
ness of the flexors of the ankle, but even in the early stage 
the loss of power in the thigh muscles and those of the hip 
is greater, and as the disease advances the preponderance of 
their atrophy becomes more and more manifest. Yet in this 
lad these muscles have good power, while any flexion of the 
ankle-joint is impossible, not from contraction of the calves 
but simple failure of the flexors. The feet can be moved 
inwards and outwards, and the movement outwards by the 
peronei is a distinction from the "peroneal form" of muscular 
atrophy, which, moreover, is believed not to be a true myop- 
athy. Peculiar as is the distribution of the weakness, the 



DISTAL MYOPATHY. 



^33 



symptoms in the face and neck associate it with other forms 
and compel us to regard it as of the same nature, an example 
of what we may term ''distal myopathy." 

It is indeed remarkable how many symptoms, small we 
may regard them, link together the various forms of myop- 
athy, and how important therefore is their recognition. Not 
less remarkable is the way in which the general type is main- 
tained in families in which several cases occur, and hardly 
less important are the variations from the type which indi- 
vidual cases frequently present. These variations leave the 
general character of the malady clear, and yet they connect 
one type with another. I wish I could show you another 
case, which affords a pertinent illustration of this connection 
— so pertinent indeed that I must tell you the chief features. 
The distal form, with weakness of the hand only, which I 
have just shown you, presents a marked contrast to the facio- 
scapular form in which the shoulder muscles and upper arm 
muscles suffer chiefly. But in the case I refer to, the affection 
of the face is slight, and instead of it the hand muscles have 
suffered, in addition to those of the scapula and upper arm. 
She is a girl of twenty-three, the seventh of a family of eleven, 
all of the same sex, a fact to note. Three of them — the first, 
second, and fifth — suffer from a similar disease; three others 
died in early life ; four are healthy.* Their parents were not 



* Mr. H. Burland of Finedon, has kindly furnished me with some par- 
ticulars of the family of the case last mentioned. Not only does it consist of 
eleven girls and one boy, but the mother was one of a family of twelve girls; 
all of the girls, except herself, died in early Hfe. Of the patient's sisters, in 
one, now thirty years of age, difi&culty in walking was first noted at fifteen 
after measles, weakness of the arms only at twenty-seven. She can now walk 
only with much difiiculty. Movements of the hips and knees are weak, so 
are flexion and eversion of the ankle, but inversion is strong. The knee- 
jerks are absent. The flexors and extensors of the hands and fingers are 
weak but not much wasted. The upper arm muscles are small and feeble, 
but not the deltoid. The trapezii, serrati, and latissimi are all wasted. The 



134 MYOPATHY AND A DISTAL FORM. 

related, and no like disease can be heard of in the family. 
Yet the affection of four sisters shows how such a vital ten- 
dency may be congenital in a family, though not inherited. 
In the patient difficulty in raising the toes was first noted at 
sixteen, and weakness in the arms at eighteen. The affec- 
tion of the shoulder girdle and upper arm was precisely that 
of an advanced case of Landouzy form. The notes state 
that ''little trace remains, in substance or in power, of the 
trapezii, serrati, latissimi, or pectorales. The upper arm 
muscles are thin and feeble, especially on the right side; the 
deltoids retain some substance. Equally great, however, is 
the affection of the distal muscles. We find no trace of the 
supinator longus. The flexors of the wrist and fingers retain 
some power; the extensors hardly any. Even the interossei 
are shrunken and very weak; if the first phalanges are pas- 
sively extended, the others can only just be straightened by 
an effort. The metacarpal bone of the thumb can be well 
bent back, but no extension of its phalanges is possible." 
Everywhere, I may say, electric excitability was diminished 
with power, and alike to each current, as is the rule in 
myopathy. Thus in the upper limbs the condition was that 
of the scapulo-humeral form, but there was an unusual de- 
gree of affection of the distal part of the limb. 

In the legs the affection was almost hmited to the muscles in 
front of the lower leg. The movements of the hip and thigh 
were good and strong, and the knee-jerks active. Thus the 



clavicular part of the sterno-mastoid is good. The orbiculares palpebrarum 
are feeble, the frontales strong. In the other sister, now twenty-five, weak- 
ness in walking was noticed at thirteen, after sore throat. In her the fron- 
tales have no power -and the orbiculares are weak, and both parts of the 
sterno-mastoids are small. The muscles of the shoulder, elbow, and hand 
are all good, but there is some impairment of free movements. In the legs 
there is very httle weakness, but the knee-jerks are absent and there is much 
inco-ordination. The nature of this case is thus doubtful. 



PATHOLOGY AND TREATMENT. 135 

affection of the legs was purely distal, as in the boy I have 
shown you; the proximal muscles were normal. In the arms 
the affection was both proximal and distal. Yet these two 
cases are linked together, and connected with other forms by 
the common features I have mentioned. 



Pathology and Treatment. 

I have spoken of all these cases as myopathic maladies, as 
muscular abiotrophy, the result of a defective vital endur- 
ance, inherent in the embryonal tissue from which the mus- 
cular structures of the body arise — a defect variable in dis- 
tribution, in character, and in tendency, but essentially the 
same in all. In a few cases trifling changes have been found 
in the nervous system ; in most it has been absolutely normal, 
both nerves and central structures, even by the latest methods 
of research, and in cases of most prolonged duration and 
profound degree. This fact seems efl'ectually to dispose of 
the hypothesis that the muscular affection is in any way the 
result of the trifling changes that have been found in a few 
cases, or the more considerable atrophy of the spinal nerve 
cells found in one case. When we remember the fact, which 
I pointed out in the last lecture, that abiotrophy is met with 
in the nervous system, in various structures, and of various 
course, it is strange that it is not more often met with as an 
associated state. It is not surprising, moreover, that shght 
secondary changes should be met with in the spinal cord 
when there has been prolonged secondary spinal curvature, 
with all its effects on the circulation. Such trifling changes, 
met with in a few cases, irregular in seat and distribution, 
can have no real significance. Yet they have been thought 
to suggest that some day it may be discovered that the mus- 
cular condition depends, after all, on a morbid state of the 
spinal cord. This idea is a rehc of the old fancy, for it was 



136 MYOPATHY AND A DISTAL FORM. 

nothing more, that there are in the spinal cord special trophic 
centres for the muscles apart from the motor cells of the 
anterior cornua. It is a doctrine that should have died of 
inanition long ago; purely hypothetical, every definite fact 
is opposed to it. 

The vitality of the muscles presents a strange duphcity. 
Perhaps it is not so mysterious as it seems at first view; the 
same double relation may be seen, I think, elsewhere, although 
less clearly. The nutrition of the muscle depends on that 
of the nerves through which its function is called forth. If 
the nerves slowly degenerate, so does the muscle; if rapidly, 
from descending irritation, the muscles undergo speedy com- 
plete degeneration. Yet the muscle has a hfe which we may 
call organic, belonging to it as a structural entity, in conse- 
quence of which it may undergo morbid changes, apart from 
the nervous system, and may fail to live on, though the nerves 
preserve an unimpaired vitality. This failure is what I have 
called muscular abiotrophy — failure of nutrition from de- 
fective vitality — and for brevity we call it myopathy. 

The treatment of this condition is a narrow subject, yet not 
unimportant. Its importance is positive and negative; to 
know what we cannot do and what we can. Life itself is 
beyond the influence of medicinal agents. Some degenera- 
tive changes seem to be within control, at least in slight de- 
gree, but it is otherwise with those vital tendencies which 
seem inherent. We can discern no clear evidence that they 
can be thus influenced; we can perceive no positive effect 
from the administration of medicine of any kind, and no 
faster failure when such agents are omitted. Yet even vital 
energy is not altogether beyond indirect influence. There is 
one agency, but only one, w^hich has a sure effect on the vital 
nutrition of the muscles, and that is their voluntary use, their 
stimulation through the nerves with which their nutritional 
integrity is so mysteriously bound up. That is the lesson 



PATHOLOGY AND TREATMENT. 137 

taught by all true muscular growth, by the disciples of San- 
dow, as by every athlete. The apphcation of the lesson to 
these diseases is all-important; it is seen alike whether it is 
enforced or disregarded. 

Muscular exercise, adapted in degree to the muscular 
state, is the one agent which distinctly stems the ebbing tide 
of life, and hinders the failure of muscular strength and mus- 
cular nutrition. Neither electricity nor massage can exert 
more than a small fraction of the influence of voluntary use. 
Without it no definite effect can be observed from their em- 
ployment; with it they seem sometimes to do a little good, 
and upward massage promotes the circulation in the muscles 
and the renewal of the blood plasma, from which their nutri- 
tional elements are derived. But that is all we can say. 

When contractures or any accidental causes arrest the 
voluntary use of the muscles for even a few months, the weak- 
ness and the wasting increase rapidly, and speedily reach a 
degree from which there is no recovery. Contracture occurs 
readily in the muscles in which there is much increase of con- 
nective tissue, especially in the calf muscles, but the tendency 
to it varies. In some cases it prevents standing and walking 
long before this would be lost from the weakness of the mus- 
cles of the upper leg. Then the division of the Achilles 
tendons is imperative. I have mentioned * one case in which 
this contraction occurred so early, in such degree, that at five 
years of age the ability to stand would soon have been lost 
from this alone; tenotomy enabled the patient to walk until 
twelve, and then again became necessary. It preserved the 
abihty for years; at twenty the patient could still walk three 
miles. 

When the contraction occurs late, and the weakness of the 
muscles of the knee and hip is great, the question may arise 

* " Pseudo-hypertrophic Paralysis," Case 35, and p. 55. 



iS^ MYOPATHY AND A DISTAL FORM. 

whether the rest the operation entails will not augment the 
weakness, so that the effect of tenotomy is useless. But the 
rest need be but brief, and its effect may be lessened by 
movements while lying. If the contraction is not extreme it 
may be diminished without tenotomy by an apparatus I de- 
vised some years ago,* in which elastic traction on leather 
around the foot is made from leather around the leg, the two 
being united by a narrow piece behind the heel; this bends, 
but has sufficient vertical resistance to prevent pressure on 
the skin, which, if continuous, so soon becomes intolerable. 
Worn during rest and indoors, the effect of the very gentle 
constaut elastic traction is most remarkable. 

At the knee and hip the contraction is of the flexors, and is 
the speedy consequence of posture which involves flexion of 
these joints as the patient sits or hes. It usually attends a 
degree of weakness which precludes any prospect of good 
from operation. It emphasizes only too strongly the impor- 
tance of maintaining as long as possible the upright posture. 
When the patient can only sit, not only do these contractions 
of the hip and knee occur, but the weakness of the muscles of 
the trunk induces inevitably an inclination to one side, which 
leads to curvature of the spine, with all its consequences on 
the movements of the chest, and the disposition to chronic 
changes in the lungs by which most sufferers find the end of 
general life. 

Elsewhere, in the arms especially, the essential element in 
treatment is the same persevering efforts to maintain the 
exercise of the muscles. For this gentle gymnastic exercises 
are extremely useful, especially the various apparatus for 
developing the muscles of the arms. But it is difficult to 
secure the necessary perseverance without the incentive 
which games provide. Fencing, indeed, is a most effective 

* " Clin. Lect." ed. 1895, p. 194. 



PATHOLOGY AND TREATMENT. 139 

exercise when the faihire of the arms is sHght, if the exertion 
is moderate and the object kept in view. Cychng gives some 
exercise to the arms as well as to the legs, and a tricycle 
is often practicable and most useful when a bicycle cannot 
be ridden. Lawn tennis involves too severe effort to be com- 
monly available, but its degraded indoor form of ping-pong 
necessitates the varied but gentle use of many muscles, which 
makes it far more than a mere game to sufl'erers from this 
disease, and it is additionally useful if played in the open air. 
When the movements of the hand begin to be impaired, the 
action of playing the piano is very useful, and the art should 
be acquired in anticipation of its need, that the pleasure 
should be an incentive to exercise, as it can scarecly be in the 
stage of laboured acquisition. 

It is the case with all measures which merely hinder a pro- 
gressive malady — their influence, however great, is unobtru- 
sive. It is negative and not positive. How real and im- 
portant it has been is only perceived when it ceases. The 
speed with which the malady then advances reveals the eft'ect 
that had been unnoticed. The sufl'erer and his friends are 
inapt to reahze these negative results, and prone to think 
that no good is done because no improvement is perceived. 
We may do something to save them from this error, and 
we must be careful not to fall into it ourselves. We should 
also do our best to try to save them from efforts to obtain 
good from the many straws held out for hope to grasp at, 
which are magnified by promise into rods of rescue. Those 
who promise with assurance that which cannot be, always 
find too readv credence, as is often discovered onlv too late. 



LECTURE V. 

METALLIC POISONING. 

Delivered at the National Hospital for the Paralysed and Epileptic^ on October 22^ 

I go I. 



Gentlemen: — Metallic poisoning has occupied a consider- 
able amount of public attention during the last year. The 
epidemic of arsenical poisoning caused by the contamination 
of beer, and the consternation it produced, will be fresh in 
your minds. Many of you may also have noted the efforts 
which have been made to lessen the amount of lead-poisoning 
incidental to the process of glazing pottery, and the difficulty 
there is in practical prevention. Cases of lead-poisoning that 
occur in local trades appeal to the public by their concentra- 
tion and by the apparent possibihty of their prevention. But 
that which is met with in such industries is but a triffing pro- 
portion of the whole amount in the kingdom, most of which 
occurs among those who are engaged in the work of renewing 
for us the freshness and fairness of our habitations — the 
house-painters. 

Lead. 
Here, for your observation, are two patients suffering from 
the effects of lead on the nervous system, and I wish to avail 
myself of their presence to impress upon you some facts 
regarding metallic poisoning. Some of them they illustrate, 
others they do not. Both patients exemplify the fact I have 
just mentioned — both are house-painters. One presents the 

140 



LEAD. 141 

characteristic effect of the disease — wrist-drop and paralysis 
of the extensors in the forearms — and the other does not. I 
think I may assume that you are famihar with the features 
of this paralysis, and I need not describe them in detail. 
Some points will come before us presently. But the case 
to which I would first and specially direct your attention 
is that of the patient who has no paralysis. He can move 
his hands freely and well, but he is suffering from various 
symptoms of feebleness of the nervous system. He is weak 
generally, although, as you see, he is fairly nourished. He 
can only walk with difficulty, but there is some cause for 
this, as we shall see. He complains of numbness at times 
in the right foot and left thigh. He has had much headache, 
and when he holds his hands out they present fine tremor, 
to which we must return. His difficulty in walking is partly 
due to an injury long ago. In 1888 he sprained his right 
ankle so severely as to be in the Bristol Royal Infirmary for 
four months. Some weeks after his discharge he injured the 
instep on the same side. The injury seems to have led to 
disease, because he returned to the infirmary and some bone 
was removed. Contraction in the calf must have followed, 
for the Achilles tendon had afterwards to be divided. Sub- 
sequently a toe was removed — why we do not know. He 
slowly recovered and was at last able to resume work, 
but after working for some time he again lost strength and 
his left leg became thin. His weakness culminated in an 
attack of colic. This was six years ago; only after a long 
period of rest did he gain enough strength to resume work, 
with, after a time, a similar result. After another attack 
of cohc a year ago, he was so much more feeble that he had 
to give up and has not worked since. During the last year 
he has also suffered from much headache and from the 
trembling of the hands. The weakness of the legs has also 
become so much worse that he was only able to walk with 



142 METALLIC POISONING. 

crutches until he came into the hospital seven weeks ago. 
Yet apart from the tremor, there is httle that is objective 
to correspond to his disability. His knee-jerks are rather 
active, but he presents no foot-clonus. His left leg is thin 
and his foot shows traces of the operations he has undergone. 
His muscular strength is small and movements are rather 
jerky and not sustained. When I first saw him he had been 
carefully examined and notes had been taken. I was told 
that it seemed to be a case of "simple neurasthenia." I 
looked casually at the bed-card, and at once my eye was 
caught by the record of his occupation, ''Painter." I looked 
from the bed-card to his gums, and there I saw written in 
equally distinct characters the record of the effect of his 
occupation — in a conspicuous lead-line. Further inquiry 
elicited the fact of the two attacks of lead-colic which I have 
mentioned, one six years ago and one a year since, but also 
that he had never suffered from any degree of wrist-drop. 

Let me interrupt my special subject for a moment, to 
consider the diagnosis that had been made. The history 
of the word "neurasthenia" is noteworthy. It is a con- 
tribution to medical nomenclature which we owe to our 
transatlantic brethren, and it attained universal use with 
the utmost celerity. The concise and concrete character of 
the word gives it a satisfying definiteness. This depends to 
a large extent on its classical and somewhat graceful sound. 
Not only is it graceful to the ear, but it is grateful to the 
mind of the patient who suffers and longs to know from 
what, who longs to have a name for that which he, or more 
often she, feels must be a more definite malady than is sug- 
gested by the common-place designation of "nervous weak- 
ness." How far its practical utility, which, if low, is definite, 
has influenced its use I cannot say. But its use has extended 
far beyond the needs of the patient, and indeed did so from 
the first. It has firmly established itself in current clinical 



" NEURASTHENIA." 143 

terminology. But it often tends to be too satisfying. Men 
are apt to rest on it as they would not on its English equiva- 
lent. If they do not actually think that they have found 
the malady from which the patient is suffering, an influence 
is often exerted on them of which they are unconscious, 
which lessens the tendency to go further in the search 
for the whole morbid state. Words are our servants, but 
they often exert a very masterly influence upon us, none 
the less effective because we are not conscious of it. They 
have also their own vitality, feeble or vigorous, and we have 
little power to influence their career. This fact has come 
distinctly within my own experience. I have to confess to 
the authorship of two words. One, ''myotatic," was always 
a puny infant, and I doubt whether it still maintains an 
independent existence. The other, '^ knee-jerk," instantly 
attained universal use, and, indeed, I think has seemed to 
most persons to have sprung spontaneously from the thing 
itself, without suggestion — perhaps the greatest compliment a 
word can pay its author. But the general use at once achieved 
by "neurasthenia" was in spite of a strong objection to it 
which was felt by many. The Royal College of Physicians 
of London could not include it in their "Nomenclature of 
Disease," and yet it is now one of the most common of 
medical words in every language. It would be instructive 
in more than one way to have a careful study of the forces 
which have influenced its career, but that I cannot attempt. 
We must, I think, admit that not only is it a satisfying word 
to those who suffer, but it has a certain convenience which 
has almost compelled many to employ it who at first ob- 
jected. If I may be pardoned for a partial paradox, its 
convenience is not the less real because this rests on features 
that are illusory. Remember that the word is a name which 
should have little meaning, even to those who use it. You 
may employ it to collect the symptoms of the case under a 



144 METALLIC POISONING. 

general designation, but do not let it cover them as a 
cloak. 

But we must come back to our patient. When we had 
ascertained the facts I have mentioned, it was impossible 
to doubt that the man was the subject of lead-poison- 
ing or that his symptoms of nervous weakness had the 
same origin. They had developed after he had passed 
from the hands of the surgeons and had gained strength 
enough to resume work. On each occasion, it was after 
he had been at Avork for some time that he began to 
fail, lost strength, and suffered from the symptoms you have 
heard, and each relapse was attended by the colic which 
demonstrated the action of the toxic influence to which his 
work exposed him, and emphasised the relation of the re- 
newed weakness to this influence. That this influence is 
the effective cause of his symptoms, little as they would 
themselves suggest it, is shown by his history, and it is con- 
firmed in an instructive way by careful observation of his 
state, especially by two features. The tremor he presents, 
which I will ask you to observe carefully, is a fine tremor 
which occurs only on movement, but it differs from the 
tremor so often seen in hysterical and nervous persons. 
That is a general irregular movement of the hand and 
fingers. Here you will observe that there is a quick lateral 
movement of the fingers, the result of contractions in the 
interossei. This is a peculiar and unusual feature, sug- 
gesting a special cause. Tremor is well known to be a 
result of lead-poisoning, and you know that it is a charac- 
teristic of the toxic influence of another metal — mercury. 
The second indication that he is still suffering from the 
influence of lead on the nervous system is very curious. 
It has been before observed, at least in Germany, but oppor- 
tunities for detecting it are rare, and are still more rarely 
utihsed. You are famihar with the wrist-drop, which is a 



LEAD. T45 

common effect of lead, the atrophic paralysis of the extensor 
muscles in the forearm. A good example of it is presented 
by the second patient before you. Such wrist-drop is due 
to neuritis and is accompanied by the characteristic "reaction 
of degeneration " to electricity — loss of faradic and increase 
of voltaic irritabihty, and to the latter a change in polar 
response. In health, contraction occurs to a weaker current 
with the kathode, the negative pole, than with the anode, 
the positive pole. In the reaction of degeneration this order 
is reversed, the contraction occurs more readily with the 
anode. In this patient we found this polar change in all 
the muscles that would be affected in wrist-drop and in no 
others, although it was the only change in reaction that 
could be detected. All the other muscles of his limbs, in- 
cluding those of the legs, presented the normal order of 
response. I am sorry — I was going to say — that you cannot 
see this. He has improved so much during the last few 
weeks that, on one side, the order of polar response has become 
normal, and on the other side, is on the way to be so, for the 
response is now equal to each pole. When he came in, the 
lead in his system must have exerted a definite influence on 
the nerve-endings in these muscles; he must have been on 
the verge of wrist-drop. This condition thus affords us addi- 
tional evidence of the present action of lead on his nervous 
system. 

My object in showing you this case is that it may impress 
on you the great variety of symptoms to which lead may 
give rise, and the importance of not overlooking the cause in 
consequence of the equivocal character of the effects. The 
variety of disturbance of the nervous system which may be 
produced is very great. Indeed, you might be prepared for 
this when you remember how wide and severe are the effects 
of acute lead-poisoning, how gravely the brain itself suffers 
in some cases, manifested by what is called "saturnine 
13 



146 METALLIC POISONING. 

encephalopathy," often attended by optic neuritis. In more 
chronic cases the symptoms seem to depend on the momen- 
tum with which the poison acts, and on the predisposition 
which the individual possesses. Let me enumerate some 
of the effects which I remember to have met with. Lead 
may cause not only the common peripheral neuritis but a 
slower chronic atrophy of the muscles, seen first in the 
interossei; it is precisely like spinal atrophy, and probably 
such, but differing in that it does not progress if its cause 
ceases to act, although it is far more enduring than the wrist- 
drop; it may be permanent, though it does not increase. 
Lead may cause some forms of sclerosis of the cord, usually 
slight in degree ; it may cause optic nerve-atrophy; and many 
forms of functional disorder may result from it. It may 
cause tremor, as you see in this patient ; chronic convulsions, 
like those of epilepsy; and hysteria, with its varied mani- 
festations, in predisposed subjects. Neuralgia, sometimes of 
great severity, may be due to it, and headache is a frequent 
effect, as well as the symptoms of general nervous weakness. 
In all such cases, in which there is nothing in the symptoms 
to suggest the cause, this may escape you, unless you are put 
upon its track either by the occurrence of other associated 
cases of lead-poisoning, by the occupation of the patient, 
or by the presence of its great sign, the lead-line on the gums. 
Let me dwell briefly on the line, because thereon hangs 
one of my lessons. It is typical in proportion as it approaches 
Euclid's definition of length without breadth, always pro- 
vided it is black. It is said to be blue, but I have never 
myself been able to see any colour in it. It is not always 
to be seen, and often it is not to be seen readily. You know, 
or should know, the reason why it may be absent even in 
the most pronounced cases. It is the edge of a deposit 
of sulphide of lead beneath the inner surface of the gum, 
where this is separated from the teeth even in a very slight 



LEAD. 147 

degree. The sulphur comes from albuminous substances 
which decompose there. Sometimes you see a similar de- 
posit in the mucous membrane of the lower lip, when there 
is tartar on the teeth with which it comes in contact. Tartar 
contains organic substance mixed with earthy salts from the 
saliva, and it yields enough sulphur to act on the lead. We 
have not this deposit in the patients here to-day. But I 
should like you afterwards carefully to compare the line 
which is present in each. In the first it is conspicuous, but 
it is not continuous; it is in separate pieces, where the gums 
are more detached. The second patient has always been 
particular about his teeth and careful about cleanhness — 
hence the detachment of the gums is shght ; and although the 
line is present everywhere it is extremely narrow and only 
seen on looking closely. Indeed, it was altogether missed 
at first. When looking for a lead-line use your ophthalmo- 
scope lens, which I presume you are never without. Careful 
as this patient has always been, he must have gradually 
accumulated lead in his system, but his final breakdown, 
with the wrist-drop which you see, he attributes to a cause 
which it is well to note. He ascribes it, apparently with 
reason, to the work of painting some ceilings. In this work 
the man who paints has to stand below that which he is 
painting, and it is impossible for him to avoid inhahng some 
of the spray which his brush necessarily throws off — spray 
which may be loaded with lead. It is the most perilous form 
of house-painting. I wish that the rich who indulge in the 
luxury of painted ceilings knew at what price it has to be 
paid for, not by them, but by those who produce the special 
beauty they desire. I think that house decorators ought to 
make the fact known to those who ask for this superfluity, 
for such it certainly is. 

But I have not quite done with the lead-line. Far more 
common than the rare cases in which it is absent, are 



148 METALLIC POISONING. 

those in which it exists only in fragments, often much 
smaller and fewer than in this patient. It may be at only 
two or three isolated spots, or on the tips of the projections 
of gum between the teeth. It can then only be found by a 
most careful and thorough search, on the upper jaw as well 
as the lower. Remember that the smallest fragment, if 
distinct, is as significant as the most extensive deposit. A 
year or two ago a patient came to me from the other side of 
the world and said that he was suffering from muscular 
wasting. I found considerable atrophy of the muscles of 
the forearms, but it was of the muscles that suffer in lead- 
poisoning, with characteristic wrist-drop as its result. No 
others were affected. They had lost faradic irritability and 
presented very little voltaic irritability, but this is common 
after a time in such cases, if voltaic electricity has not been 
applied. The excitabihty to voltaism quickly improves in 
this state after a short course of treatment with it. The 
onset had been subacute, just as it commonly is from lead. 
Of course, I at once examined his gums. At first sight they 
seemed normal, but on more thorough inspection, and espe- 
cially on examining the gums of the upper jaw, several spots 
were found at which there was a slight separation from the 
teeth, and there I found two or three indubitable fragments 
of lead-line. I afterwards also found some black points at 
the ends of the projections between the teeth of the lower 
jaw. I could ascertain no source for the poisoning. The 
patient was a grocer, but had not for years been accustomed 
to handle the lead-paper by which tea is protected. Still, 
I could not doubt that he was suffering from simple lead- 
palsy, and I therefore felt justified in giving him a very 
hopeful opinion, a prospect of steady although slow improve- 
ment under treatment. The forecast was entirely justified. 
He went home in a year's time almost well. But I should 
not have spoken so plainly, perhaps, had I known what he 



LEAD. 149 

afterwards told me. After I had expressed my opinion he said 
that he had been sent to England as a sort of forlorn hope. 
He had been told that he was suffering from progressive mus- 
cular atrophy which nothing was likely to arrest. His own 
words were that he started under what he "felt to be a 
sentence of death." Perhaps he exaggerated. It is always 
well to remember the advice once given by a wise physician: 
"Never believe anything a patient says that another doctor 
said." But if he had told me this before, I should have 
been less emphatic in a statement which was evidently a 
contradiction of that which had been told him. I should 
have given him some hope and should have allowed this to 
be gradually augmented by his experience. It is always 
desirable to avoid expressing a difference of opinion more 
strongly than is absolutely necessary. And I heard of it 
again; I heard of it from his country, after his return. But 
I cannot doubt that the cause of the palsy might have been 
discovered by a sufficiently minute search, and it is to im- 
press the importance of this upon you that I tell you of the 
case. It is an illustration of one of the wise sayings which 
the late Sir William Jenner was wont, I might almost say, to 
stick into the minds of his pupils, "More mistakes are made, 
many more, by not looking than by not knowing. " 

But there is one last resort for the detection of this cause 
of palsy. If the symptoms are such as to suggest lead, and 
you are sure that there is no trace of lead-line in any part of 
the gums, you may feel confident that it is not at work, pro- 
vided the state of the gums is such as would certainly give 
rise to it. If the gums are everywhere perfect you cannot feel 
thus sure. I have seen saturnine wrist-drop without a trace 
of line, because the gums were in perfect apposition to 
the teeth; there was no room for doubt; the case was one 
of the many which once occurred in Sheffield in consequence 
of the solvent power of peaty water upon leaden pipes. Yet 



I50 METALLIC POISONING. 

we have a source of information. If the case is seen early, 
its nature may be decided by an analysis of the urine, espe- 
cially after iodide of potassium has been given for a few- 
days. It is a rather troublesome process, needing a large 
quantity of urine, but it may be decisive. I remember em- 
ploying it in one case of wrist-drop perfectly like that of 
lead in distribution, course, and character. The result was 
negative, and its negation proved only too trustworthy; the 
extensor palsy was followed by wasting elsewhere and by gen- 
eral, rapid, progressive muscular atrophy. 



Arsenic. 

I mentioned arsenic as another metalHc poisoning which 
has loomed large in the pubhc and professional eye. The 
extensive epidemic of arsenic-poisoning in the north has had 
at least one good result — a vast increase in the general pro- 
fessional knowledge of the subject, so that the facts which 
were previously familiar to a few are now known to all. 
But it may still not be quite useless for me to impress on you 
the need for fixing its signs on your mind, ready for revival, 
because the need for the knowledge may come when you 
least expect it. Like lead, it causes neuritis, but arsenical 
neuritis usually affects the legs before the arms, although 
the latter suffer in severe cases. Moreover, its effects 
on the nerves vary much; the common palsy may be 
absent, and the sensory nerves may suffer much or most, 
and hence the symptoms may be equivocal and even mis- 
leading — sometimes, indeed, they may be identical with those 
of tabes. 

Just as the line on the gums is the indication of lead, 
changes in the skin, especially certain forms of pigmentation, 
constitute the outward and visible sign of the influence of 
arsenic, visible at least if you look for them, and a sign if 



ARSENIC. 151 

you know what they are Hke. They have been abundantly 
described, not only by Dr. E. S. Reynolds, of Manchester, to 
whose perception of their significance we owe the discovery 
of the cause of the epidemic, but especially by Dr. H. G. 
Brooke and Dr. Leslie Roberts, who have published a very 
full account of them and their pathology in the "British 
Journal of Dermatology" for April, 1902. I only propose to 
mention some salient points regarding the pigmentation, 
points that have come frequently under my own notice. 
Other changes are also common, especially the thickening 
of the skin of the palms and soles, but the pigmentation is 
that which is likely, as a rule, to attract attention, and is 
of most practical importance. Moreover, this Hospital is 
the only place at which you are at all likely to become prac- 
tically acquainted with it. Arsenic alone enables us to pre- 
vent or lessen the troublesome eruption which bromide 
causes, and few patients who take the combination for more 
than two years escape pigmentation. In one case I was able 
to discern the precise amount which had been effective. The 
darkening of the skin was first distinct when the patient had 
taken liquor arsenicalis for two years in uniform quantities, 
and the total was 104 grains of arsenious acid, or one grain 
weekly. Doubtless slight signs of it might have been dis- 
cerned sooner. But I think that if you look at the neck of 
many old cases of epilepsy attending here, you will meet with 
an example before long. The change is most marked on the 
skin of the trunk, front and back, but it extends to the limbs 
and also to the neck, where indications of it may be detected 
with least inconvenience. Given with bromide, arsenic has 
very little tendency to act upon the nerves, even when a 
sufficient amount has been taken to cause extreme pigmenta- 
tion. I have a strong impression that it is most readily pro- 
duced in those who are most prone to the bromide acne, but 
the impression must of necessity remain such, because the 



152 METALLICiPOISONING. 

disposition to the acne leads to the administration of larger 
doses of arsenic. 

The impunity with which arsenic can be taken with 
bromid, and the peril that attends a far smaller amount 
in beer, is very remarkable. The only explanation I can 
offer is that alcohol augments, and bromid restrains, the 
metabolism in the nerves and therefore the tendency for 
arsenic to replace the phosphorus and impair function and 
nutrition. 

Whether or not you are able to become acquainted with 
the aspect of the skin that is due to arsenic, it may serve 
you in good stead if you remember its occurrence and also 
its chief features. The brown pigmentation begins as small 
spots, which may commence, as I have seen, in spots of con- 
gestive redness, and the brown tint succeeds the red. These 
dark spots sometimes exist alone, more often they are seen 
chiefly on the outer portions of the most pigmented regions, 
where the tint is more uniform. The uniformity may be 
due to coalescence of the spots, but sometimes this diffuse 
colouration seems the first thing. The tint is that which is 
called sepia, a warm sepia or cold sepia, according to its 
duration, to use the terms employed by artists. It is not 
so dark as the pigmentation of Addison's disease, and has 
not the same distribution. Although it is more marked at 
places at which there has been pressure, it occurs irrespectively 
of this and is greatest on the parts of the trunk least affected 
in Addison's disease. When the small discrete spots coalesce, 
they often leave small areas which are unpigmented and 
which have a pearly whiteness. Three weeks ago I saw a 
patient whose skin over the whole trunk was of a deep ma- 
hogany colour from this disease, with such w^hite spots scat- 
tered over it. He was so prone to the bromide rash that even 
the dose of arsenic he was taking (seven minims with 25 
grains of bromide twice a day) did not suffice to keep him 



ARSENIC. 



153 



entirely free. But he had been free from fits for 16 months 
and his parents would not hear of a reduction in either 
the bromide or the arsenic. The darkening of the skin, they 
said, was quite unimportant, and that is the common opinion 
of those who present it when they know its cause. I have 
constantly to explain to patients its origin, and to give them 
the choice between the bromide spots and the darkening of 
the skin ; there is never hesitation in choosing the latter. The 
white spots I have mentioned are common and somewhat 
characteristic, although they are met with in other forms of 
pigmentation. They have been called "rain-washed" spots 
from their scattered distribution, but their whiteness suggests 
a more potent agency than simple washing. I believe that 
their pearly whiteness is not the effect of contrast alone, but 
that they are actually paler than the normal skin. Why 
such areas should not only resist the pigmentation but should 
apparently lose what they possessed, is a mystery which the 
pathologists have not, I think, explained. But we may note 
that there seems to be a curious solidarity in these pigmentary 
processes, in consequence of which excess may entail adjacent 
deficiency and, I may add, a deficiency may be attended by 
adjacent excess. 

Perhaps you will allow me to digress for a moment to 
mention to you a very remarkable illustration of the latter 
fact — increased pigmentation in the vicinity of its diminution. 
I have mentioned the case elsewhere,* but it will probably be 
new to you. It is that of a man who had traumatic meningeal 
haemorrhage over the left hemisphere. As a result of this, 
during the three days he lived after the injury, the right, 
opposite half of the hair of his head and of his brown 
moustache and beard became blanched so as to be almost 
white. The change was watched during hfe and care- 



* Manual of Diseases of the Nervous System. 
14 



154 METALLIC POISONING. 

fully noted after death. It was like that which has been 
described as the result of profound emotion, but it was due 
here to a physical agency. It can only be explained by 
assuming that the disordered innervation so changed the 
secretion at the roots of the hair as to produce a material 
capable of ascending the hairs and discharging their pigment. 
But after death we noticed another thing, which leads me to 
mention the case. The very grey, almost white, right half of 
the beard was separated from the brown left half by a narrow 
vertical line, or narrow zone, in the middle line, in which 
the hair had become almost black. Apparently where the 
disordered influence ceased in its extreme degree, at the 
blending of the innervation of the two sides, a change in the 
pigmentary process had occurred of the opposite character. 
Mysterious as the fact is, and perhaps impossible to explain, 
it illustrates the close relation between the plus and the minus 
in pigmentary processes. I am not sure that wx may not 
find another illustration of this in some cases of atrophy of 
the pigment of the choroid adjacent to a spot at which it 
is collected, and also in the heaping up of pigment in asso- 
ciation with areas of atrophy. But this may have another 
explanation. 

To return to my proper subject. I desire especially to fix 
in your mind the fact of the occurrence of this characteristic 
pigmentation. Whether or not you are able to become 
actually acquainted with its appearance, it may chance to 
be as useful to you as it was to me last year. Last February 
a young Indian civil servant, a district magistrate, was 
brought to me by his family medical attendant. He had just 
arrived in England with symptoms of extensive peripheral 
neuritis, so severe that he could not stand or walk without 
assistance. There was much weakness of the legs as well 
as wasting of the muscles. There was incoordination and 
absence of the knee-jerks, considerable fibrillation in the 



ARSENIC. 155 

wasted muscles of the thighs, and great diminution in elec- 
trical excitability, which also presented a peculiarity with 
which I need not now^ trouble you. There w^as also consid- 
erable impairment of sensibility to pain and touch. His 
hands hkewise were weak and very unsteady. The illness 
had followed a sharp attack of intermittent fever two or 
three months before, and he had previously suffered badly 
from the ordinary malarial fever in India. Such neuritis is 
well known as an occasional sequel to these malarial fevers, 
caused apparently by a toxin which is left in the system. 
But in that form the muscles of the lower legs are chiefly 
affected and incoordination is seldom a prominent symptom. 
When I came to examine the patient's body I found it covered 
with pigmentation perfectly Hke that of arsenic. Indeed, I 
could not doubt its nature. Of course, I questioned him 
carefully regarding any possible source of arsenic-poisoning, 
and especially whether he had taken any tonic containing 
arsenic. It seemed certain that he had not, and no accidental 
source could be ascertained. Thus the sequence of events 
suggested malarial influence as the cause, but it was im- 
possible to misinterpret the declaration so clearly wTitten on 
his skin of the influence of arsenic. Moreover, another fact 
was learned which gave support to the cutaneous message. 
About the time of the commencement of his illness he had 
an attack of shingles. It is a long time (35 years) since Mr. 
Hutchinson pointed out that herpes zoster may be caused by 
arsenic. Hence we were compelled to consider that his con- 
dition was due to this, in part or altogether; the facts wxre 
too definite, although inexplicable, and we treated the patient 
accordingly. Six weeks later the medical attendant wrote to 
me that the mystery was cleared up. News had been re- 
ceived from India of the discovery of a prolonged attempt 
to kill the patient and his family by the habitual introduction 
of arsenic into their food. Several members of the family 



156 METALLIC POISONING. 

had suffered severely and the nurse had actually died from 
the poison. Our patient improved steadily, and I saw him 
a fortnight ago practically well, able to walk fairly and cycle 
30 miles. The ataxy had vanished; some blunting of sensi- 
bility on the front half of the soles alone remained. He will 
soon return to his work in India. What is of particular in- 
terest, because it relates to a point about which we know 
little, is that the arsenical pigmentation has almost disap- 
peared. 

Another pertinent instance of the revelation which this 
sign may afford, I need only allude to, because I have already 
described it in my first series of Chnical Lectures under the 
heading "Mistaken Diagnosis." The patient came with what 
seemed to be characteristic symptoms of ordinary tabes — 
pains, ataxy, and loss of knee-jerk. He came when I could 
not properly examine him, so I ordered him some medicine 
containing arsenic and arranged to see him again in a month. 
Then when I stripped him to test his sensation, to my con- 
sternation I found his skin covered with typical arsenical 
pigmentation. He was a colour-merchant, accustomed to 
deal in various pigments, but he had also taken for a long 
time a tonic pill containing arsenic. Both these cases illus- 
trate the tendency of the sensory nerves to suffer under 
arsenic far more than under lead. The patient recovered, 
and he taught me another lesson. There is evidence that 
iodide of potassium promotes the elimination of arsenic as 
well as of lead. The path by which it can pass away is, of 
necessity, the blood. You know that it is not well to give 
iodide freely to a patient with recent and severe lead poisoning, 
because the lead stored in the tissues may be thrown into 
the blood too suddenly. This case showed that we should be 
equally cautious in the case of arsenic. Iodide in very mod- 
erate doses led to such an increase in the symptoms of 



ARSENIC. i^y 

irritation of the nerves as to compel its discontinuance for a 
time and very gradual resumption. 

I have only one other instance to mention to you and that 
is an illustration of the other side of the shield. An epileptic 
patient, a young woman, about 30 years of age, presented 
marked pigmentation from the arsenic taken with bromide. 
From the latter she was deriving great good. I explained 
the nature of the darkening of the skin and she was satisfied. 
About six months later I received a letter from her sister 
written in dire distress. The aspect of the skin had caused 
two medical men to assure her that the patient was certainly 
the subject of Addison's disease — a progressive incurable 
malady. I could only reply that the patient when I last saw 
her presented darkening of the skin due to the arsenic. I 
heard no more of the case. It is right to say that this was 
before the Manchester epidemic had its opportunity of exert- 
ing its educational influence on the profession. 

The facts I have given you are commonplace. Many of 
them may have been known to some of you, some of them 
may have been known to many of you; but one fact I am 
sure is true of all my hearers — for it is as true of myself as 
of anyone — the commonplace is, of all knowledge, that which 
we can least afford to despise or to disregard. 



LECTURE VI. 

SYPHILITIC DISEASES OF THE NERVOUS 

SYSTEM.* 

Delivered at the Medical Graduates' College and Polyclinic, October, igo2. 



Gentlemen: — I have been asked to lecture to you at short 
notice, but fortunately a subject has been assigned to me — 
syphilitic disease of the nervous system. I have not, how- 
ever, been told what to say. The subject far transcends the 
limit of a single lecture. All I can do is to present for your 
consideration some general principles concerning the most 
important practical branches of the subject, those which 
should guide us in the prognosis and treatment of these 
diseases. 

I fear I can only give you that which is old. But the 
old is not, as such, to be despised. It has been well said 
by Ribot, as to senile failure of memory, that ''the new 
perishes, the old endures." The saying is true in a much 
wider application, although it is only a partial truth. We 
may also remember another aspect of the relation. To pre- 
sent old knowledge to new minds involves a constant renewal 
of its youth. The seed that is" old produces a new plant. It 
may be true that "there is nothing new under the sun," but 
there is a sense in which it is also true that there is nothing 
which is not new. The rising sun is old enough, but each 
sunrise is a new event. 

* " British Medical Journal," April 4, 1903. 
158 



INCIDENCE. 159 

Even in my restricted topic I must confine myself to the 
principles which seem to me of most importance. First, 
however, we must have a clear perception of what we are 
deahng with when we speak of ''syphilitic disease" of the 
"nervous system." What do we understand by ''nervous 
system" ? If we only mean the actual nerve cells and fibres, 
the functional elements, I might paraphrase that chapter in a 
book on Iceland which Dr. Johnson said he could repeat from 
memory, the chapter on Icelandic snakes. Doubtless you 
know^ your Boswell, and remember that this feat of memory 
turned out to be the repetition of the sentence — "Throughout 
the whole of Iceland there are no snakes." So I might say, 
"there is no syphilitic disease of the nerve structures." But 
the term "nervous system" includes also the neurogha, 
which supports and separates the nerve elements, the blood 
vessels, which penetrate and permeate the centres, and the 
membranes, which enclose and protect them. These struc- 
tures are among the most frequent seats of the morbid pro- 
cesses of constitutional syphihs. The nerve elements proper 
do indeed undergo degeneration after syphilis, but this is a 
different condition. I will refer to it presently, but it is not 
within our special subject. 

I have not made this comparison with the snakes of Ice- 
land merely to enunciate a paradox. Behind it lies an impor- 
tant fact. Syphihtic disease of the nerve centres, developing 
in what may be termed the "adventitial" elements, produces 
symptoms for the most part through the changes it causes in 
the nerve elements themselves. But these are simple, not 
specific. They are secondary to the syphihtic disease, but 
they are the same as would be caused by any other disease 
of the same character, whatever its nature. The significance 
of this fact is far reaching. Specific treatment acts only on 
the specific process. It has no direct influence on the sec- 
ondary changes by which the symptoms are produced. This 



i6o SYPHILIS OF THE NERVOUS SYSTEM. 

fact should be kept in view in all your practical conclusions, 
and to impress it upon you is one of my chief objects to-day. 

Let me give you some illustrations. You may not need 
them, but, believe me, the art of getting the knowledge you 
have not, is to welcome that which you think you have. 

To take first a salient example of the simple nature of the 
process by w^hich syphilitic disease causes symptoms — con- 
sider syphihtic disease of a cerebral artery. The disease 
narrows the vessel, or narrows the orifice of a branch which 
arises at the affected spot, but causes hardly any symptom 
until a clot suddenly forms. The narrowing makes the flow 
sluggish in the "backwater" just beyond the diseased spot; 
at last, clot forms on the altered wall and quickly closes 
the vessel. It extends on, up to a branch from which a col- 
lateral supply can maintain the circulation; if there is none it 
spreads to the distal twigs. The region of the brain from 
which the blood supply is thus suddenly cut oft", at once loses 
its function. Unless a collateral flov\^ can be established in 
an hour or two, it perishes, undergoing necrosis, "necrotic 
softening," of necessity enduring, with persistent loss of 
function. But the thrombus which forms is simple, not 
specific, and so is the resulting softening. The only syphilitic 
process is that in the wall of the artery. 

Reduce the disease of the artery to a cicatricial state as 
quickly as you can by treatment, you cannot change its 
effects. You can exert no more influence on the thrombosis 
or on the softening than in a case in which the softening is 
due to embohsm. Nor can you influence the characteristic 
symptoms which are due to these simple effects of the disease. 
This must be clear to you, but it is not so many years since 
I heard a man of professional distinction say of such a case 
of sudden syphihtic hemiplegia, "Oh, he has a node within 
the skull; give him mercury and he will get all right." 

Sometimes the course of the case seems to verify such a 



ORIGIN OF SYMPTOMS. i6i 

favourable prognosis. Under due treatment the symptoms 
lessen and may pass away. They do so in the same manner 
and degree in many cases of embolism from heart disease, 
and do so whether medicine is given or not. The initial 
effects of any vascular lesion are much wider than those 
that are permanent, because the area of brain disturbed is 
greater than the area destroyed, and the permanent symp- 
toms depend on the functional importance of the latter. 

Take, again, the case of a syphilitic gumma growing from 
the membranes of the spinal cord. It slowly compresses the 
cord and this causes paraplegia. The effects on the cord are 
precisely the same as would be produced by any other kind 
of tumour. If pressure is slowly exerted, the fibres lose all 
power of conduction long before they suffer total destruction. 
Secondary degeneration may follow with all its symptoms, 
and yet certain elements of the fibres may retain such con- 
tinuity as permits their ready renewal when the pressure is 
removed. Conduction, if it has not been lost too long, may 
be restored when treatment causes the compressing growth to 
shrink, just as it is slowly restored when a sarcoma outside 
the cord is removed by a surgical operation. But the treat- 
ment does good, not by its influence on the changes in the 
spinal cord, on which the symptoms directly depend, but by 
acting on the specific cause of those changes. These pass 
away if there has not been actual destruction. 

Such syphilomata may form on the sheaths of the cranial 
nerves and produce the same efi'ects — arrest of function, with 
palsy in the part supplied, recovering when the compressing 
agent is removed. It is so, also, with the similar processes 
in the membranes of the brain. But here, as in the nerves 
and the membranes of spinal cord, the processes of growth 
are associated with another process — that of inflammation. 

The subject of syphilitic inflammation brings before us 
some pathological conceptions which it is important to dis- 



i62 SYPHILIS OF THE NERVOUS SYSTEM. 

cern. The characteristic specific process is neoplastic, the 
formation of tissue which, when recent, is semigelatinous in 
aspect ("gummatous"), and resembles, histologically, granu- 
lation tissue. After a time it becomes firmer, and two changes 
occur. Its elements become transformed to fibres, which 
contract in a cicatricial change, or they undergo fatty degener- 
ation and caseation. This caseation occurs in several dis- 
crete spots, perhaps because the vessels of the neoplasm 
become thickened and closed. These areas may coalesce, 
but do not constitute the general uniform caseation so charac- 
teristic of a tuberculous mass. This caseation in several foci, 
combined with the gummatous aspect of the recent parts, is 
the most characteristic feature of these specific growths. 

Every process of tissue formation, whatever its nature, 
involves vascular disturbance proportioned to its acuteness. 
Syphilomatous tissue always forms rapidly, and the attendant 
vascular disturbance constitutes a state of active congestion, 
and even of inflammation. 

Thus we can trace the two elements, the inflammatory and 
the neoplastic, in all syphilitic processes. In proportion as 
they are acute the inflammatory element preponderates. We 
meet with foci in the meninges, which we should call inflam- 
mation, but for the amount of gummy tissue produced, which 
may be such that in places the characteristic spots of casea- 
tion are seen. We may be then in doubt whether to call it a 
gumma with adjacent inflammation, or inflammation of a 
gummatous character, and it is really a choice of terms. But 
it is doubtful how far the inflammation itself is specific or is 
simple. 

Inflammation is a curious process. You know how 
it spreads in some structures when once lighted up. We 
sometimes see this in the peritoneum in a terrible degree. 
In the cerebral membranes an inflammation once excited, 
by whatever cause, tends to spread swiftly in proportion to 



ELEMENTS. 163 

its acuteness. In proportion to this, the inflammatory ele- 
ment predominates in syphihtic meningitis, and in that pro- 
portion it has the features of simple inflammation. It speedily 
becomes extensive, general, and even may be bilateral. It 
seems as though some form of morbid agent had the power 
of exciting inflammation which at once attains a degree far 
in excess of its cause. It seems also to be less amenable to 
treatment in proportion to its acuteness, in proportion to the 
degree in which the simple inflammation runs away, as it 
were, from the specific cause. We meet with instances of 
this, happily not often, in the cerebral membranes. We 
meet with the same, more frequently, in the spinal cord. 

Acute myelitis, focal or transverse, is met with so often 
in the early stage of constitutional syphilis that it is impossible 
to doubt a causal relation. Yet the inflammation presents 
the same features, and runs a course quite the same, as in 
patients in whom syphilis can be excluded. Remember that 
in all acute inflammations of organs, the proper functional 
structures undergo rapid destructive changes which are 
regarded as a participation in the inflammation. But these 
are simple in aspect, similar in every form of inflammation 
equally acute. They are intense in proportion to the inflam- 
mation, and may speedily attain a degree from which re- 
covery is slow, imperfect, or impossible. This is conspicuous 
in these cases of acute myelitis, and they justify the inference 
that in these cases also the symptoms depend on the simple 
effects of the specific element. It is ahke true whether the 
inflammation is purely such, or Avhether the damage to the 
nerve elements is brought about by disease of the arterial 
walls at the spot affected. In the more chronic forms of 
local inflammation, in which the process passes into that 
which may be termed sclerosis, the same fact is apparent. 
The morbid process is interstitial, and the nerve elements 
suffer secondarily. 



i64 SYPHILIS OF THE NERVOUS SYSTEM. 

Local chronic inflammation of the cerebral cortex has 
other effects which are also due to the simple damage to 
the nerve elements in the cortical substance. Even if the 
effects of inflammation pass away, no structure is ever quite 
the same as before, and in the grey matter of the brain a 
slight residual alteration may entail a grave change in func- 
tion. Instead of stimulated, proportioned liberation of nerve 
energy there is spontaneous discharge which gives rise to 
local convulsion. This may occur from the irritation of the 
active inflammation, but also as a residual effect, such as 
might be due to the inflammation caused by a blow. It also 
is a manifestation of simple changes on which specific treat- 
ment can have and does have no influence. 

The points I have mentioned are not matters of theoretical 
pathology; they are of the utmost practical importance. On 
your perception of the mode in which the symptoms are pro- 
duced depends the correctness of the forecast you can form, 
of the prognosis you can give. The essential point is that 
the specific process can be influenced by treatment, but this 
can produce no effect on the simple changes on which the 
symptoms directly depend. The forecast is favourable in 
proportion as the latter can pass away when their cause 
ceases to act. Hence it is important that you should culti- 
vate the habit of picturing to yourselves what is the exact 
morbid state, and strive to discern the nature of the changes 
which give rise to the symptoms. Endeavour to acquire the 
habit of forming such a mental picture. Obtain all the data 
you can, and then strive to see with your mind's eye, and 
trust your vision. It may seem difficult at first, but will 
become easier with practice. It will often serve you in good 
stead in many forms of disease, in many parts. 



PROGNOSIS. i6s 



Prognosis. 



The application of these facts to prognosis should be self- 
evident. The prospect of improvement and recovery depends 
on the extent to which, after the removal of the specific 
disease, the simple processes on which the symptoms depend 
can pass away. In all tissues the tendency to recovery is 
great, if the change has not proceeded to actual destruction. 
Thus you will perceive that in arterial obstruction there is 
a speedy, permanent destruction of tissue, and function can 
only be regained in so far as it is capable of compensation by 
the other hemisphere, or in the degree in which initial damage 
exceeds actual destruction. In the case of slow compres- 
sion the possibility of recovery depends partly on its degree, 
and still more on its duration. Pressure always involves 
secondary inflammatory changes in the compressed tissues. 
These go on to cicatricial processes if the pressure has been 
long continued; in time they constitute a grave hindrance, 
sometimes an insuperable obstacle, to the restoration of con- 
tinuous structure and conducting function. Paraplegia from 
such pressure may be complete for a month, and recovery 
will probably, in time, be perfect. If complete for three 
months, recovery may possibly be perfect, but is more likely 
to fall short of the normal state; but if complete paraplegia 
from compression has endured for six months only partial 
recovery can be expected after even the complete removal 
of the cause, and after a year the return of function may 
be very shght, and at best will not be great. Of course, 
these are but rough assertions; they are, I believe, approxi- 
mately true, but they are given chiefly to fix on your minds 
the importance of considering duration in the attempt to 
forecast the future of a case. You have doubtless long since 
learned by experience, that may have been painful and cer- 
tainly must have often been trying, the urgency with which 



1 66 SYPHILIS OF THE NERVOUS SYSTEM. 

a patient, and still more the friends, desire to know the 
future course of the malady. They expect from us a pre- 
science more than human. It seems reasonable to them 
that we should be able to see into the future with the same 
certainty as into the past, and the same confidence as into 
the present. We are fortunate when the conditions are such 
that we can give them that which they ask for; but you will 
only discredit yourselves in the long run by holding out 
confident hope when it is unjustified. Strive, then, to per- 
ceive the morbid state, and if you cannot anticipate much 
improvement, it is seldom that you cannot hold out hope of 
some, but take care that you are clearly understood, and that 
your "may" is not construed as "will." 

It may seem strange to some of you that any cases of this 
character should lose their chance of complete recovery by 
reason of their long duration before appropriate treatment is 
employed. But it seems to be a law of Nature that every- 
thing that never should be, sometimes is. One cause is be- 
cause some patients suffer long before they seek advice. It is 
not so with paralysing maladies, but it is so sometimes with 
those that damage nerves, and even with arterial disease so 
placed as to cause only slight symptoms for a long time 
before arrest of the circulation is produced, and when the 
parts affected are those to which no motor functions are 
related. It is not often, now, that such disease is undetected 
in consequence of the ignorance of the doctor who is con- 
sulted, but it happens sometimes because he does not make 
a sufficiently careful search to discover slight but conclusive 
symptoms of organic disease. Among these optic neuritis is 
one of the most important and most frequently overlooked. 
Indeed, I may say in passing that no defect in medical educa- 
tion seems so persistent as ophthalmoscopic training. It will 
be so until the inspection of the normal disc is part of prac- 
tical physiology, or at least is taught with the stethoscope at 



PROGNOSIS. 167 

the beginning of practical medicine. Clinical work abounds 
with unused opportunities, because the eye is never looked 
into until the end of the student's course. 

Another frequent reason for the prolonged unchecked 
development of the disease is a belief that it cannot be. One 
of the great lessons of life— sometimes only learned late — is 
hesitation in pronouncing anything impossible. Certainly, 
this disease is sometimes met with under conditions which 
suggest that it is impossible, especially to those who know 
the patient best. One fact, at any rate, you should always 
remember. It can be excluded only when there has never 
been exposure to possible infection in the common way. If 
there has been, if it has been escaped by "luck" — its denial 
should have very little influence on your opinion. You know 
also how constantly its occurrence in married women has no 
symptoms to make it suspected, and it is important to re- 
member that the evidence afforded by children may be ab- 
sent. Indeed, the subject is one in which it is important 
never to forget the rule — a rule of almost universal applica- 
tion — that the absence of evidence is of very little value com- 
pared with that of its presence. Nature is unveracious as well 
as man, or rather seems so because our ears are tuned only 
to its affirmations. Its ''no" is often altogether untrust- 
worthy, but this is because we interpret its silence as negative 
without the least justification for doing so. Almost every 
common symptom of a morbid state is sometimes absent; 
every indication of a common cause is sometimes absent. 
Hence assurance is possible only when the common cause 
can be absolutely excluded. 

Thus the practical lesson which follows from the perception 
of these facts is that the cause of the symptoms of the various 
syphilitic diseases which damage the nervous system is a 
secondary result of the specific process. Remove the latter 
by treatment, remove it as completely as possible; the secon- 



i68 SYPHILIS OF THE NERVOUS SYSTEM. 

dary effects may pass away, or may only lessen, or may persist 
with only slight diminution. A cicatrix from a gumma in the 
liver may be unimportant ; in the nerve centres it may cause 
enduring symptoms. In the cortex of the brain organic 
epilepsy may be its result; in the deeper centre, permanent 
palsy. Even a gumma pressing on the cord may be removed 
by treatment too late to prevent a degree of mischief which 
cannot pass away, and some palsy may be enduring. 

Remember also that the actual result of treatment on the 
specific process depends on its duration. The new formation 
rapidly diminishes in size under treatment. Apparently the 
tissue elements that are of recent formation, chiefly cellular, 
undergo granular disintegration, the results of w^hich are 
quickly removed; but the older cells undergo a change into 
fibres, which may perhaps also be formed between them, and 
the diminution in size is partly due to the progressive cica- 
tricial contraction of this fibrous tissue, which proceeds to 
such an extreme degree. Treatment seems to promote this 
cicatricial process in the tissue elements which have attained 
too mature a stage to undergo disintegration and total re- 
moval. But this process has its own consequences; that 
which it entirely surrounds suffers inevitable constriction, 
which may perpetuate or even augment the effects of the 
active disease. This is another reason why your prognosis 
in cases that have proceeded unchecked for some time, should 
be very cautious. 

In a previous lecture, I pointed out that this change, 
going on all round the wall of an artery, seemed to have 
induced its occlusion, and that this effect had apparently 
been promoted by the influence of the treatment which 
arrested the disease and helped the cicatricial change. Hap- 
pily such annular disease is rare, whether in a nerve or in 
an artery, and the conducting function of a nerve may be 
slowly restored in spite of considerable enduring constriction. 



PROGNOSIS. 169 

Yet the impairment may continue long after cicatrization of 
function is established. This fact seems to be incompre- 
hensible to many. As long as symptoms continue, as long as 
the normal state is not regained, it is believed that there must 
be specific disease unconquered; treatment must be made 
more energetic, must be repeated. Iodide is continued and 
increased; course after course of mercurial inunction is em- 
ployed. Sometimes all is to no purpose; sometimes there is 
the slow natural recovery we know so well when causal disease 
has ceased, a recovery then inevitably assigned to the per- 
sistent treatment employed, although it may be, I believe, 
in spite of it. You may ask. Is not this reasonable? Are 
we not justified in our inference, since we cannot see what 
is going on ? 

Well, I would ask you to consider what you do in other 
conditions that are beyond the direct range of observation. 
You infer from that which you can directly discern the 
character of the process you cannot actually perceive. If a 
patient comes to you with a recent node on the tibia you 
know that under iodide or mercury it will have disappeared 
in six weeks. If the node has existed for six months, at the 
end of six weeks it will have become much less, but peri- 
osteal thickening will still be felt, and this will be very slow in 
disappearing. It will lessen in time, just the same whether 
or not you continue specific treatment. The residual thick- 
ening is due to cicatricial tissue, which must persist after all 
the specific element is removed. So with a syphilitic ulcer of 
the skin. At the end of six or eight weeks' treatment — if this 
is adequate — all the pecuhar specific thickening is gone; the 
ulcer may not be healed, but all that remains is a simple 
ulcer undergoing simple cicatrization, which will go on just 
as well if you do not continue specific treatment as if you do. 

When the ulcer is healed, what remains? A scar, first 
hvid, afterwards brownish, in which the skin is thinner and 
15 



lyo SYPHILIS OF THE NERVOUS SYSTEM. 

smoother than elsewhere — a scar which remains to the end of 
Hfe. In every tissue it is the same. Every morbid process 
leaves its changes in proportion to its degree and character. 
A destructive process leaves cicatricial tissue in place of 
normal structure, and this may even surround a cavity if 
there has been a massive destruction. Simple inflammation 
may leave a slighter change, but usually such as to be dis- 
cerned, at least by the microscope, and this degree is colossal 
compared to the changes in finer nutrition which must always 
ensue. The effect on function, even of the slightest residual 
change, is enduring, and important in proportion to the 
delicacy and differentiation of function of the structures 
affected. Hence, whenever the nerve structures are damaged 
by specific processes, we should be prepared for imperfect 
recovery, however successful our treatment of the primary 
process may be. It is indeed remarkable how great is the 
restoration of function in many cases, in the course of time. 
But the fact I wish to impress upon you is that the "time" 
is not occupied by the removal of the specific disease, but 
by the recovery of the damaged structures when this has been 
removed. 

You will perceive from what I have said that the path- 
ology, prognosis and treatment of these maladies are closely 
connected, or rather they are the same, viewed from different 
sides. You can only frame a forecast by discerning whether 
the causal disease can be removed completely, and how far 
the nerve elements can recover. For this purpose it is essen- 
tial to form a mental conception of the process I have men- 
tioned. When you cannot see with the eye you must strive 
instead to see with the mind. The great difference between 
various processes will then rise clearly into view, and all 
that the difference entails. 

For the most part the symptoms of these processes are 
hardly ever really slow in their production. They are sub- 



TREATMENT. • 171 

chronic, subacute, acute, or sudden, reaching a considerable 
degree in less than three months, and often in much less. Of 
all it is true that the more rapid the development of the 
symptoms, the less is their course affected by specific treat- 
ment. Those which are most deliberate are chiefly the result 
of a gumma, compressing or irritating, or of gummatous 
inflammation of the membranes. Over these, treatment ex- 
erts its greatest influence, and in them the prognosis is the 
best, subject to the limitations I have mentioned — long dura- 
tion and irritative influence. The acute symptoms, acute as 
distinguished from sudden, are for the most part the result 
of inflammation. This, although excited by a specific cause, 
varies in the relative amount of inflammation proper, which 
is greater the more acute the process. The nerve structures 
suffer chiefly from this, and the more rapidly the symptoms 
develop the greater is the destructive implication of the nerve 
elements, the less is the room for the influence of specific 
treatment. We see this strikingly in the cases of acute trans- 
verse myehtis, so frequent in syphihtic subjects, in whom, as 
I have said, it runs a course differing in no respect from 
that which it pursues in other patients. The cases of actually 
sudden onset present a course over which specific treatment 
can have and does have no influence. I need not repeat 
what I have said regarding this point. 



Treatment. 

It may seem strange that the therapeutic progress of the 
last half century has left us without any new remedy for 
syphihs. But we need not be ashamed of the nineteenth 
century, since it has produced the second of our two certain 
•remedies, iodide. Its value was discovered in the thirties, 
and in England. Like the majority of our most useful drugs, 
its service was found by empirical observation, indeed, it may 



172 SYPHILIS OF THE NERVOUS SYSTEM. 

be said, almost by accident. The real or supposed influence 
on goitre of burnt sponge, led to the discovery that it con- 
tained iodine, and to the use of combinations of iodine for 
other swellings, among them for nodes. From this the step 
was small to the discernment of its power over other syphilitic 
processes, a power as certain as it is mysterious. 

The older remedy, mercury, has come down to us from 
the dim distance of a thousand years. Its use by the Arabians 
is said to have been anticipated in India, but the Orient 
shrouds in impenetrable mist the beginnings of all things. 
Its service in syphihs is believed to have been one of the 
Eastern lessons the Crusaders brought back to Europe, unless 
it had been conveyed by the Moors to Spain with skill in 
other arts, such as the Alhambra retains for us. 

The two agents stand on a different level. We have other 
facts regarding the power of mercury which make its influence 
on syphihs less strange. It is possible that it has a capacity 
of arresting many diseases that depend on an organismal 
virus, although it is only in a slow disease that we can avail 
ourselves of this effect. The fact was ascertained in the early 
days of the Brown Institution that an animal under the 
influence of mercury was unaffected by a dose of anthrax 
virus which would certainly be fatal to a similar animal not 
so protected. It is beheved to have an influence on all pro- 
cesses of inflammation. Those of our profession who have 
occasion to watch the only internal inflammations which can 
be directly observed, those within the eye, are firm in their 
belief in the influence of mercury upon them, irrespective of 
their specific nature. I may add that it has been employed in 
most of the cases of cerebral meningitis, including some 
apparently tuberculous, in which recovery has been known. 
This is, at least, true of my own experience. Mercury is a 
poison, but a considerable quantity may be contained in the 
blood, if gradually introduced, and we can understand that 



TREATMENT. 173 

this may be sufficient to be fatal to the organisms of disease 
long before it is fatal to the hving elements of the body. But 
to permit this effect the disease must be one of slow devel- 
opment. 

We can thus at least seem to understand the influence of 
mercury in syphihtic processes, and also the trust, placed 
on it in the early stage, when the organisms must be in their 
first flush of growth in a fresh soil. But iodide has no such 
toxic property. It is a salt not far removed in nature from 
common salt, yet its influence on the processes of syphihs is 
certain. This must be due to the iodine, and it is said to 
be possessed in equal degree by the combination of iodine 
with a vegetable oil, "iodipin, " or "iodinol." Iodide, in 
itself, seems almost inert on the normal processes of the body, 
and yet it has a profound influence on this morbid process. 
But Ave must remember that all these elementary bodies seem 
able to enter into combination with albuminous substances, 
modifying their influence, sometimes profoundly. A slight 
change in constitution will transform a food into a poison. 
The mystery of the certain influence of iodide is made more 
salient by our uncertainty as to its eft'ect in other morbid 
states. It has been, and is, thought to do good in many; 
but, if we search for stringent proof, we shall find ourselves 
in agreement with Nothnagel, who, in his great book on 
"Materia Medica," says: "The therapeutic influence of 
iodide is undoubted only in one condition, tertiary syphilis, 
and it is possible in hyperplastic aft'ections of the lymphatic 
glands and thyroid. In all other conditions its influence is 
doubtful and uncertain. We have employed it much, very 
much, but in other maladies we have never obtained definite 
and incontestable certainty that the improvement and re- 
covery occasionally observed were due to it."* 

* Nothnagel and Rossbach, "Arzneimettellehre." yte Aufl., 1894, p. 299. 



174 SYPHILIS OF THE NERVOUS_SYSTEM. 

Of course, its administration in many maladies must 
often coincide with spontaneous improvement, so very easily 
ascribed to coincident treatment. But when due allowance 
is made for this, and when the cases in which it has failed 
are given their weight, does the lesson of the residue differ 
much from the experience of Nothnagel ? The contrast pre- 
sented by its power over syphilitic new formations is most 
strange. Not less so is its innocuous character compared 
with the toxic power of mercury. It is difficult not to beheve 
that the future has some revelation in store for us, which may 
not only explain what is now mysterious, but in doing so 
may augment our resources, ahke in means and method. 

It is not through diseases of the nervous system that any 
new means of combating syphilis are likely to be discovered. 
Duty precludes us from the attempt. The effects of such 
disease are so grave, and are rendered graver by every day's 
delay, that we dare not pause to search for a new agent. We 
must employ at once the means we know and trust, and 
leave the task of discovery to those whose province is less 
profound. As a fact, moreover, nothing is such a hindrance 
to the discovery of new remedies, truly such, as the efficiency 
of those we have. If we know what will cure, we seldom 
dare search for another remedy. 

The difference between the two agents is familiar and 
important. Iodide can be thrown into the system in any 
quantity; mercury can only be introduced gradually. For 
the chief lesions of constitutional syphilis they seem equally 
useful. But when the process is inflammation, we should 
expect mercury to have the more certain influence, and 
observation affords some confirmation of this. It is not for a 
physician to express an opinion on the treatment of the early 
stage of the disease, but in this there is a consensus of opinion 
of the need for mercury on the part of those who can speak 
with authority. Regarding the later processes, there seems 



TREATMENT. 175 

to be a general feeling, rather than opinion, that mercury can 
do a little more, and can do it more thoroughly than iodide, 
but that the latter does its work more speedily. The feehng 
deserves respect, even practical respect, but I do not think it 
rests on strong evidence — at least so far as the nervous system 
is concerned. The opinion is largely due to the use of mer- 
cury after iodide has lessened the symptoms, and probably 
after the syphihtic process has been entirely removed. The 
damaged nerve structures have slowly regained function 
during the subsequent mercurial treatment, to which the later 
improvement has been assigned. Xo dehcate therapeutical 
inferences ought ever to be drawn from these diseases. We 
are right to apply to them all we can know or suspect, but the 
pitfalls of fallacy are, as we have already seen, many and 
treacherous. Real knowledge can only be increased from 
that which is within the range of \^sion, from the surface of 
the body. It rests with the dermatologists to augment our 
certainty, and increase our power. They can see and we 
cannot. The risks that delay involves are to them trilling. 
They should endeavour to ehminate every source of fallacy, 
to distinguish between the specific and the simple elements 
in the processes they treat, and to make their therapeutic 
observations precise, multiple, and widely known. Then we 
should feel sure of much we now only suspect, and perhaps 
we should doubt some things we now believe. 

Of one thing I am quite sure, that the symptoms of a 
syphihtic growth may diminish and pass away as rapidly if 
iodide only is given, as we can conceive possible. I do not 
affirm that it is always so, but I remember many cases in which 
10 gr. three times a day produced, in a week, cessation of head- 
ache and distinct diminution of early optic neuritis, which 
had vanished at the end of a fortnight. In one such case 
shght hemiplegia had disappeared at the end of a month, and 
hemianopia, which had been complete, was reduced to part of 



176 SYPHILIS OF THE NERVOUS SYSTEM. 

one lower quadrant. But this remained permanent in spite 
of mercury also. 

It is said that much larger doses of iodide are sometimes 
necessary, but I have not myself met with evidence of this, 
except in patients who have long been taking moderate doses. 
The use of large doses — 30 gr. or 40 gr. — has been called the 
new American system. I have already referred to the saying 
that " there is nothing new under the sun." Many years ago 
I had occasion to go through some of the old casebooks of 
University College Hospital, and I found one case in which 
Dr. John Taylor gave 40 gr. three times a day for constitu- 
tional syphilis, somewhere about 1847. The same physi- 
cian, by the way, at the same time, made constant use of the 
thermometer at that time to ascertain the presence and degree 
of fever, long before the instrument came into general use. 

I think it is not Avise to give iodide and mercury together 
in full doses, except for a short time in a very urgent case, 
when every means and measure are needed to stem life- 
threatening disease. There is reason to think that iodide 
promotes the elimination of mercury, as it does of most 
metallic substances, and thus hinders the retention in the 
system of enough to act upon the processes of the disease. 
We cannot be sure that an adequate quantity is present in 
the blood unless we have such evidence as. is afforded by 
slight inflammation of the gums. The difference in the 
readiness with which this is produced is probably due to 
differences in individual power of elimination, which seem 
to be effected chiefly by the liver. 

This explanation is, at any rate, plausible, and I think 
useful. It suggests that, if there is not the sign in the gums 
of enough mercury in the blood to act on the tissue processes, 
we should increase the dose — double it, treble it — until we 
obtain the evidence. But it is wiser not to give at the same 
time an agent which has the power of promoting its elimina- 



TREATMENT. 177 

tion, except there be the urgency I have referred to. All 
experience shows that the affection of the gums is evidence 
that enough is present in the system. It may then be stopped 
for a day or two, and continued in smaller quantity to main- 
tain the effect for three or four weeks; then the iodide may 
wisely be resumed. It will have its own effect, and may also 
at first maintain the influence of the mercury by bringing 
into the blood that which has entered the tissues. 

We cannot improve on the physicians of long ago in the 
method of administering mercury. The object is to get 
enough in the system, and this can only be slowly achieved, 
or inconvenient toxic symptoms result. One of these is 
gastro-intestinal irritation, which is always greatest when 
the administration is by the mouth. The old method was to 
rub it into the skin, and it is, I am sure, the wisest. One 
modern method is to inject it under the skin. Whether or 
not this is equally effectual, which I doubt, it is certainly 
much more uncomfortable than inunction. By the latter 
the gums can be affected in five or six days, which is as 
speedily as the result can safely be obtained by any system. 

Inunction is much facilitated by the use of the oleate, 
which is not only cleaner in aspect, but, I think, surer in re- 
sult. Order a drachm of the 10 per cent, oleate to be rubbed 
in twice a day for three or four days, and then continue once 
a day until the end of a week. If the gums then show no 
sign, resume the two daily rubbings until they do. But re- 
member one small precaution, which I should be ashamed to 
mention to you did I not know how much depends upon the 
trifles of our work. See that the same small piece of flannel 
is always used, and let the first inunction be 2 drachms. 
Otherwise the nurse will think it so much cleaner and nicer 
to take a fresh piece of flannel each time, which will retain 
more than half the dose, and you will wonder w^hy your 
patient's gums show no sign. 
16 



178 SYPHILIS OF THE NERVOUS SYSTEM. 

I do not think it matters into what part the mercury is 
rubbed. It is often convenient to have it rubbed in as near 
as you can to the affected part — close to the scalp if it is 
the brain, down the back if it is the spinal cord. This has a 
certain reason, that the oleate makes the skin rather sore, and 
thus effects slight counter-irritation. It has another reason, 
of a kind not to be despised. There is nowadays too much 
knowledge, public and popular, regarding the use of drugs 
and their purpose. Many of the laity, not alone of the male 
sex, draw an immediate inference from the use of mercury, 
an inference which is undesired by the patient. It is pre- 
vented when the site of inunction is near the seat of the dis- 
ease, and when the colourless oleate is employed, instead of 
the blue ointment with its suggestive tint. Such a device 
for the avoidance of distress does not merit any deprecation 
on the ground of high morality. If it is true that "things are 
not what they seem," it is equally true that they sometimes 
should not seem to be what they are, when the seeming can 
do no good and may do harm. 

One element in treatment I have yet to mention. I have 
left it to the last because it runs counter to the cherished 
practice of many of those who have had experience in the 
treatment of this disease. It concerns the duration of treat- 
ment. Regarding the processes of the constitutional disease, 
definitely such, my conviction is that specific treatment 
should be energetic, brief, renewed, but not continuous. By 
''brief" I mean that it should stop at the end of eight weeks 
or so, and be renewed after two, four, or six months, and that 
the patient should have three or four weeks' treatment with 
iodide every four months during the first year after any true 
specific symptoms, and every six months for the next three 
or four years. 

Let me tell you the reason for my conviction. I have said 
it before, but a teacher who hesitates to repeat, shrinks from 



TREATMENT. 179 

his most important duty, and a learner who dishkes to hear 
the same thing twice over, lacks his most essential acquisition. 
Many years ago a patient came under my care with symptoms 
of a cerebral syphiloma. Under 10 gr. of potassium iodide 
three times a day the symptoms rapidly passed away, and 
the patient seemed well. He continued, however, to attend 
the hospital and to take the medicine. At the end of three 
or four months he presented symptoms of disease of the upper 
dorsal region of the spinal cord. They progressed rapidly, 
and caused his death. It seemed impossible that the disease 
could be syphihtic, since he was still taking the medicine 
which had so speedily removed all indications of such disease 
in the brain. But the necropsy shook our confidence in the 
seemingly impossible. In the brain there was the shrunken 
relic of the gumma; in the spinal cord, invading it from the 
membranes on one side, was a similar growth, in the active 
stage, typical under the microscope, and typical also in the 
naked-eye feature of disseminated caseation, a character of 
conclusive significance. 

The lesson this case taught me I have since seen confirmed 
by other cases, not my own, however. It is that treatment 
may lose its power if continuously maintained. It is not 
altogether unintelligible that this should be. We cannot 
doubt that syphilis is an organismal disease, that it depends 
on bacilli as yet unidentified. We have yet no definite objec- 
tive acquaintance with these microbes, but the symptoms of 
the disease harmonize best with the theory that their Hfe is 
continued by germs which persist in various parts of the body 
when the organisms die. The course of the malady suggests 
that these germs may long ''lie low" and latent, but develop 
from time to time under influences we cannot discern. A 
consideration of the course of the disease and its relation to 
treatment, compels the conclusion that this has no influence 
whatever on the latent germs. It seems to destroy the 



i8o SYPHILIS OF THE NERVOUS SYSTEM. 

developed and developing organisms, and thus dissipates 
the morbid processes they excite. But the most thorough 
treatment may fail to prevent future development of the 
disease, at whatever stage it is adopted, however early. I do 
not say that it has no such preventive effect; but instances 
have been met with by every one who has had much experi- 
ence, in which there was recurrence after recurrence, in spite 
of most thorough treatment. The only reasonable explana- 
tion of this seems to be that the germs are indestructible. 
They cause no symptoms until some influence induces and 
permits their development. After a given outbreak there 
may be none left, and treatment then seems to have cured 
the disease. In another case there may be many, and then 
recurrence occurs after the same treatment. Hence, whether 
syphilis is or is not incurable as a constitutional malady, it 
is certainly one of the cure of which we can never be sure. 

Hence my belief that the essential principle of treatment 
is that it should be energetic but not continuous. Energetic 
mercurial treatment is, of course, such as to affect the gums, 
and this cannot well be continued for more than six or eight 
weeks, nor need it be. Iodide can be given persistently in 
large doses for many months with no grave constitutional 
inconvenience, and I know that such long continuance is 
thought by some to be an essential element of thorough treat- 
ment. But the germs seem able to become acclimatized 
to the presence of the iodide and to develop in spite of it. 
The fact is not unintelligible. Dallinger found that a tem- 
perature which surely killed certain organisms, failed to hinder 
the vigorous development of their germs, if successive broods 
were gradually inured to heat, which was increased by slow 
degrees. So we can conceive that the syphilitic germs may 
gradually become accustomed to the presence of iodide. 
Even then, it is true, a great increase in the dose may arrest 
their development. But the increase cannot proceed indef- 



TREATMENT. i^i 

initely, and the question is, Is this long-continued treatment 
needed? My own conviction is that after eight weeks of 
adequate treatment the specific disease is at an end. All 
that remains is the non-specific element in the process, or, 
especially in the case of the nervous system, the secondary 
simple effects in the nerve elements, which can only pass 
away slowly, and sometimes cannot pass away completely. 

Thus the nerve elements suffer simple changes in con- 
sequence of the specific process adjacent to them, changes 
which are not directly influenced by the treatment of the 
latter. In the same way they may suffer simple degenera- 
tive changes, not as the direct effect of adjacent specific 
disease, but as a mysterious sequel to constitutional syph- 
ilis. These also are not influenced by specific treatment. 
They are the post-syphilitic or para-syphilitic degenerative 
diseases, of which locomotor ataxy and general paralysis of 
the insane are the most frequent forms. They are primary 
degenerations, such as we know to be caused by chemical 
poisons, organic and inorganic, and they are probably due 
to a toxin, the result of the previous presence of the organ- 
isms of syphihs. Similar effects may follow a more acute 
organismal disease — diphtheria. We cannot doubt that 
the relation of these maladies to syphilis is similar, that the 
constitutional disease induces a perversion of some part of the 
chemistry of the body so that a poison results, perhaps with 
the help of other morbid influences — a poison that endures 
long afterwards. The evidence is purely that of sequence. 
In the case of diphtheria, which may cause symptoms iden- 
tical with those of post- syphilitic tabes, the mechanism has 
been definitely proved, and this analogy gives great weight 
to the evidence of sequence. But, just as it is not patho- 
logical, so it is not therapeutical. Most tabetic patients have 
iodide given, and hope is held out of benefit, but the cases 



i82 SYPHILIS OF THE NERVOUS SYSTEM. 

are very few in which even sHght improvement can be traced. 
A large majority are sure they derived no benefit, and not, 
a few are certain that it did harm. The same is true of 
mercury, except that energetic treatment seems more often 
to be productive of distinct deterioration. We should not, 
indeed, expect evidence from treatment. The only sure 
antidote to diphtheria has no influence on its paralytic 
sequel. 

But you should know that these toxinic degenerations 
sometimes develop before the true constitutional disease is 
at an end, while gummata and gummatous inflammation 
still occur, for which specific treatment is needed. The 
important fact is the combination of symptoms produced 
and the difficulty of discerning their causes. In early dis- 
tinct tabes, paralysis of ocular muscles may occur, which 
may be of the nature so common in tabes, or may be due 
to a syphiloma of the nerve or specific neuritis. Still more 
perplexing are the cases to which Erb's attention has lately 
been specially directed, in which specific spinal pachymenin- 
gitis has coincided with true tabetic degeneration. If the 
nature of syphilis is such as I have suggested — if germs 
are deposited in the system which develop from time to time 
under influences of which we know nothing — it is easy to 
understand that the organismal processes, truly syphilitic, 
due to later germs, should coincide with degenerations which 
are the effect of toxins, the result of earlier broods. 

Let me remind you, however, of one useful criterion of the 
existence of post-syphilitic degeneration which is often of 
service when you are puzzled by symptoms which may be 
due to either process. This is the isolated light-inaction of 
the iris — ''isolated" because it still acts readily on accommo- 
dation. You are familiar with this, which is known by the 
name, as just as it is cumbersome, of the "Argyll-Robertson 
symptom." You know its association with tabes and general 



TREATMENT. 183 

paralysis as degenerative sequelae of syphilis, but you may 
not know that it is met with in association with other con- 
ditions, and also as an isolated symptom. Even then, it is 
of great significance as an indication of old syphilis, and I 
have many times had reason to appreciate the guidance it 
has afforded. 

But these degenerative conditions are not w^ithin my 
present subject and I have reached the hmit of time at my 
disposal. I have endeavoured to put before you some gen- 
eral principles which should be kept in mind. If you strive 
to apply them to cases that seem clear, you will find it easier 
to use them in cases that are obscure. It is necessary to 
accustom yourselves to analysing the symptoms in simple 
cases, and discerning the grounds on which the prognosis is 
founded and the treatment based, in order to obtain the 
ability to do so in cases that are complex. Even those that 
seem most difficult will generally yield to a deliberate effort 
to apply to them the principles I have given you; they will 
yield, if not altogether, at least in a degree sufficient for 
immediate need. Moreover you will, I believe, seldom fail 
to find that your conclusions are confirmed, and your treat- 
ment justified, by that to which we have all to look, 

" The balance in the hand of time." 



LECTURE VII. 

INEVITABLE FAILURE. 

A STUDY OF SYPHILITIC ARTERIAL DISEASE. 

Delivered at the National Hospital for the Paralysed and Epileptic^ October 22, 

1901. 



Gefitlemen: — Patients sometimes die when we expect them 
to Hve. The discrepancy between our forecast and the fact 
is, of course, the result of our ignorance. It is occasionally 
impressed upon us in a special manner when death termi- 
nates the reticence of life, and we are permitted to read the 
record of disease, and yet cannot solve the mystery. Some- 
times, however, a careful scrutiny reveals to us the reason for 
our error, and when it is so, we can often learn many lessons. 
It is to an instance of this that I desire to direct your atten- 
tion to-day. One of the lessons that it teaches is ahke 
startling and unexpected. It is the evidence that the best 
and wisest efforts to prevent death probably promoted its 
occurrence, and could not but do so. They did not cause it, 
for it was, by the nature of things, inevitable, although the 
malady was such as is usually counted curable, and com- 
monly is so. These are the facts of the case. 

A girl, aged 25, a waitress, w^as admitted, after having 
suffered for three months from headache, which was severe 
from the first, and was referred to the front and back of the 
head. After it had existed for a month, vomiting was added 
to it, and both symptoms continued. Towards the end of 

184 



SYMPTOMS. 185 

another month she was noticed to become strange in man- 
ner, and the mental disturbance increased, so that she is said 
to have been "always talking nonsense." Soon afterwards, 
three weeks before admission, some loss of power of the right 
side was noticed, which was thought to have commenced 
suddenly, but it subsequently increased. She also had a fit 
of some kind. The only other fact of importance is that a 
doctor, who knew something about her but does not seem 
to have treated her for this illness, stated that she had prob- 
ably had syphilis. She was an ill-nourished, anasmic girl, 
very weak, and in a condition of stupor. She did not speak, 
or do what she was told, although she could evidently see 
those about her, and resented examination. There was 
considerable right hemiplegia, weakness of the right side of 
the face, complete paralysis of the upper arm, although she 
could move the forearm and hand a little; power in the leg 
was limited to slight movement of the foot. The left limbs 
were moved freely. There was also foot-clonus on the right 
side; sensation was impaired in the right Hmbs but not abol- 
ished; the optic discs were normal. 

Those are the essential features she presented. Inunc- 
tions of mercurial ointment were ordered, a drachm twice a 
day. For a few days there was distinct improvement: she 
moved the hand better, and became able to answer questions. 
It w^as not, however, greater than we often see from the first 
influence of the rest and suitable food a patient receives in 
the ward of a hospital. The improvement soon ceased, 
and she became duller and feebler. At the end of a week 15 
grs. of iodide of potassium, three times a day, was added to 
the mercury. But in a few days more the increase in weak- 
ness was so distinct that the inunctions were stopped, the 
iodide being continued alone. She continued in much the 
same condition for another fortnight, the stupor indeed in- 
creasing, and the movement of the right hand becoming less. 



i86 INEVITABLE FAILURE. 

She had several slight convulsive attacks, some affecting 
only the right side. The optic discs continued free from 
any trace of neuritis. At the end of three weeks after ad- 
mission, paralysis of the left side came on almost suddenly, 
complete. The stupor deepened to coma, the temperature 
rose to 104°, and three days later, on the twenty-sixth day 
after admission, she died. 

The symptoms suggested a rapid cerebral growth. The 
prolonged headache, afterwards associated with vomiting, 
was especially significant of this. The course of the symp- 
toms before admission was that which is met with from an 
untreated syphilitic tumour. Sudden hemiplegia is occa- 
sionally met with in the course of a tumour, especially towards 
the end, so that this fact — the alleged suddenness of the onset 
— did not seem to have much weight against the indications 
afforded by the other symptoms. Nor was the absence of 
optic neuritis a negative symptom of much significance. 
Optic neuritis is an incident in the course of a growth; it 
may occur at any period, or be absent. It is important to 
remember the general diagnostic law that the absence of a 
common symptom has small negative importance compared 
with the value of the positive indication which its presence 
affords. At the same time normal discs are unusual in a 
tumour of such rapid development, and therefore had rather 
more significance than they would have had with symptoms 
of more chronic course. 

Here was a case in which it was reasonable to anticipate 
that treatment would have been successful, if the disease were 
of the nature assumed. Grave as was her state when she 
came in, it was far from hopeless, and yet the patient died. 
What solution of the mystery did death afford ? The disease 
was found to be such as it was thought to be, so far as its 
nature was concerned, but it was not of the character sup- 
posed. It was s}qDhilitic, but there was no growth. There 



MORBID STATE. 187 

was extensive disease of the arteries, such, aHke in extent 
and in degree, as is seldom seen. The disease was most 
intense at the commencement of each middle cerebral artery, 
at the place at which the passage of the anterior cerebral 
from the internal carotid converts the latter into the middle 
cerebral. Here on each side the disease had entirely sur- 
rounded the vessel. The external prominence was very 
slight, but the thickening of the wall had encroached on the 
cavity of the artery, even to the point of obliteration. It was 
especially great on the left side, and on this the anterior cere- 
bral was Hkewise involved in the disease for some distance and 
also closed. In each middle cerebral the most intense dis- 
ease extended, lessening in degree, for about one-half to 
three-quarters of an inch, but beyond this there were scat- 
tered spots of disease, nowhere surrounding the vessel. 
Similar patches were seen on each posterior cerebral artery. 
The posterior communicating arteries were almost free. 
The left anterior cerebral, after it had turned back above 
the corpus callosum in the inner side of the frontal lobe, w^as 
smaller than the other and pale, but perhaps only in conse- 
quence of contraction from the lessened blood supply to be 
presently mentioned. A similar change was found in the 
small branches which this and the middle cerebral send into 
the substance of the brain. To this condition I must return. 
What effect had this arterial disease produced on the 
circulation within the vessels? The right middle cerebral 
was occupied by a recent clot, which extended from the dis- 
ease at its origin throughout the whole vessel. It had com- 
pletely closed it in its entire length, and there was commenc- 
ing necrotic softening in the region of the brain supplied. 
This thrombus must have been the cause of the final hemi- 
plegia — the palsy on the second side, the left, which came 
on three days before death, and caused it. The aspect of 
the clot corresponded to the duration of the paralysis; it 



i88 INEVITABLE FAILURE. 

was red, uniform, and not adherent. The state of the brain 
supphed by the vessel was that which we should expect three 
days after the arrest of the blood supply. The disease at the 
origin of the artery appeared to have quite closed it, but 
some of the contraction may have been due to the influence of 
the agent — formalin — in which it had been at first placed, 
since some blood must have passed through until three days 
before death, when the clot formed. 

In the other middle cerebral, the left, a remarkable condi- 
tion was found. There was the intense disease at its origin 
which I have mentioned, thickening the wall, and encroach- 
ing on the cavity from every side, so as completely to close it. 
Similar disease extended along the wall for three-quarters of 
an inch, gradually diminishing but continued as scattered 
spots. Where greatest, it had so completely closed the 
vessel that there was no room for clot, but adjacent to it 
was an old coagulum occupying the vessel for about a third 
of an inch. It was decolorised, adherent, its aspect such as 
would correspond to the period since the first attack of hemi- 
plegia, which you will remember was on the right side, oppo- 
site to this vessel. But the obstruction of the artery was 
complete, and the hemiplegia was incomplete! Beyond 
this thrombus the artery contained fluid blood, and there was 
no softening of the region of the brain supplied by it, such 
as usually follows the obstruction of an artery, and such as 
we found commencing on the other side, from the recent 
thrombosis in the opposite artery. The circulation had 
evidently been maintained in the distal part of the vessel. 
How had this occurred, so as to prevent the extension of the 
clot ? The answer is strange. On this side an artery arose 
from the posterior cerebral and passed forward, entering 
the fissure of Sylvius, to join the middle cerebral just 
before its bifurcation where the fissure divides It was 
a vessel of some size, although far smaller than that which 



MORBID STATE. 189 

it joined. It was free from disease, and had carried enough 
blood into the middle cerebral to prevent the extension of 
the thrombus, although of course far less than would have 
been received by the usual channel. But it was enough to 
prevent necrotic softening and complete hemiplegia, although 
it was not enough to prevent some paralysis and some in- 
structive pathological changes, as we shall presently see. 

Still more strange is it that another abnormal vessel had 
in like manner maintained the circulation in the anterior 
cerebral. I told you that this artery was involved in the dis- 
ease which existed where it arises from the internal carotid, 
the disease at the beginning of the middle cerebral. The 
anterior cerebral Avas also completely closed, and adjacent to 
the closure was an old clot, decolorised and adherent, hke 
that in the other vessel, and extending also along it for about 
one-third of an inch, just beyond the anterior communicating 
artery. Further on the vessel contained fluid blood, as did 
the middle cerebral beyond the clot in it. The reason was 
clear. Your anatomical lore should not have been so much 
attenuated by time as to make it needful for me to remind 
you that this anterior communicating artery completes the 
arterial circle at the base of the brain which you know by 
the name of our great countryman, Wilhs. This communi- 
cating artery is usually single. Here, however, it was double. 
A second artery crossed about a third of an inch in front of 
the ordinary vessel, and was equally large. The clot in the 
anterior cerebral extended beyond the first communicating 
artery, but not quite so far as the second, and through this 
the blood supply had been maintained in the distal part of 
the anterior cerebral, just as was the case in the middle cere- 
bral. As in the latter, the amount of blood brought to it 
thus was much less than the normal flow, but it was enough 
to maintain the movement of the blood, to prevent the ex- 
tension of the clot, and to prevent necrotic softening. 



iQO INEVITABLE FAILURE. 

These facts enable us to understand the symptoms better, 
and also their mechanism. The limited clot in the left 
middle cerebral, adjacent to the occluding disease,* must 
have caused the onset of the right hemiplegia, by the sudden 
diminution in the blood supply to the motor region, although 
the abnormal artery from the posterior cerebral carried 
enough blood to prevent the paralysis being complete. In 
the same way the clot in the anterior cerebral may be 
assumed to have caused the mental symptoms, although its 
effect was lessened by the supply of blood brought by the 
second communicating artery. You know how often dis- 
ease or injury of the anterior lobes, and especially of the left, 
has caused symptoms of this character. 

But this does not enable us to understand the progressive 
increase in the symptoms, the increasing palsy, the deepening 
speechlessness and stupor. Farther careful examination dis- 
closes to us the apparent cause of this — indeed, I may say the 
certain cause. Extensive change is to be seen in certain 
parts of the cerebral substance. It has been carefully ascer- 
tained by our pathologist. Dr. Collier, but you will be able 
to observe it for yourselves. In most of the region of the 
cortex supplied by the middle cerebral on the left side, and 
much of that supphed by the anterior cerebral — the vessels 
we have just been speaking of — there is a very peculiar altera- 
tion. The grey substance is shrunken; it is diminished to 
not much more than half its normal thickness. Both this 
and the white substance beneath present a peculiar granular 
aspect and definite induration. Wherever this exists there is 
found considerable change in the small arterial twigs, which 
pass into the brain substance from the branches of the main 



* The clot probably formed before the perfect closure by disease, when 
the aperture had become so small that very little blood could pass through. 
The complete occlusion immediately ensued. 



MORBID STATE. 191 

arteries. The alteration in these arterioles is very definite. 
They are contracted, small and pale, evidently in consequence 
of the diminished blood supply, since you know that arteries 
adapt themselves to their contents. But Dr. Collier finds in 
them also a process of endarteritis ; there are active changes 
between the internal and middle coats, cell proliferation 
thickening the middle coat, and still further diminishing the 
cavity. It is doubtful whether this endarteritis is syphilitic 
in nature; indeed it probably is not. A similar process has 
been found to be the mechanism by which the arterioles are 
obliterated wherever there is a considerable persistent diminu- 
tion in the supply of blood. But we can be quite sure that 
this process has been progressive; it has gone on until death, 
in spite of treatment, apparently as a simple process — the 
result of the diminished blood supply. 

The alteration in the structure of the brain must be 
ascribed to this change in the arterioles, slowly increasing 
the effect of the diminished blood supply, since the two 
coincide in distribution. Both are processes which have 
gone on of necessity, once set up by a persistent cause. 

It should now be clear why the symptoms bore so much 
resemblance to those of cerebral tumour. The severe per- 
sistent headache, afterwards with vomiting, was the result 
of the morbid process in the vessels, extensive and unchecked. 
The disease must have commenced some time — certainly 
several weeks — before the headache began. Pain in the head 
is an inconstant symptom of such disease, but it often pre- 
cedes, for a few days or weeks, the occurrence of throm- 
bosis, which, with the sudden palsy it produces, is commonly 
the first proof of the disease. The headache is very rarely 
attended by vomiting, so conspicuous here. Such suffering 
almost invariably brings the patient under treatment; it is 
seldom that the disease progresses unchecked, but the girl 
had dosed herself with various things — phenacetin, antipyrin, 



192 INEVITABLE FAILURE. 

etc. — in the hope of relieving the pain, and apparently had 
no friends to secure proper treatment when she became 
incapable of doing so herself. 

The second character by which the symptoms resembled 
those that would be caused by a growth was their steady pro- 
gress, the increase of the right-sided weakness, of the inability 
to speak, and the mental dulness, in spite of her treatment 
in the hospital. We must ascribe this to the slow changes 
in the cerebral nutrition due to the causes we have just 
considered. Both it and the narrowing of the arterioles 
were secondary effects of the occlusion of the large arteries 
at their origin. The collateral supply of blood, which saved 
the patient from the severity of the sudden symptoms, was 
insufficient for the normal circulation in the arterioles or 
for normal nutrition of the brain substance. It was insuffi- 
cient to prevent the slow development of other symptoms, 
at last equally severe, and not unlike those that would have 
been caused by a tumour, or might have been suddenly pro- 
duced by extensive initial thrombosis. From that she was 
saved by the abnormal arteries. Such abnormal vessels are 
rare, but not extremely rare. They are, however, most 
unlikely to be present in any individual case. We can never 
assume their existence, still less their situation and influence. 
We cannot allow their possible existence to determine our 
diagnosis. This we can only base on the probable, and rely 
on the principles that guide us aright in the majority of 
cases. Yet our rules are always open to correction and im- 
provement, or at least they should be. 

As I have said, the case is a rare one; but no cases can 
teach us more which is important for common use than those 
that are rare. They touch the common on every side; they 
almost compel thorough study, and this involves the per- 
ception of their general and wider relations. Let us see what 
lessons we can gain from this case; if we secure some, we 



DIAGNOSTIC PROBLEM. 193 

shall learn, unconsciously perhaps, much more. In the at- 
tempt to point them out, and especially to be clear, I shall 
have to repeat myself. I ought not indeed to apologise for 
this, for as brevity is said to be essential to wit, so repetition 
is certainly essential to effective instruction. 

I will begin with the question of the diagnosis of the dis- 
ease. You know the saying, "It is easy to be wise after the 
event"; I may add that it is not easy to be wiser. If we 
met with a quite similar case we could be accurate in our 
diagnosis — easily. But Nature is not given to repetition. To 
be wiser we must learn lessons that we can apply under con- 
ditions not the same. We must not rest content with the 
perception that error was here inevitable, but could hence- 
forward be avoided in identical circumstances. From every 
case we should endeavour to learn that which may tend to 
keep us right, whatever be the features of another case of 
the same nature. The lessons we may gain from the facts 
of this case are especially instructive, because they afford 
an instance of the way in which one symptom influences the 
significance of another, and of the need for comparing them, 
of weighing them, not only alone but together, in order to 
discern the resultant of their several forces, whether the 
mutual effect is increase or diminution. 

The first important fact is the unusual duration and 
severity of the general cerebral symptoms, which must for 
two months have been the result of the arterial disease alone. 
It is important to note this, because had the fact been part 
of our common knowledge — the fact that such disease might 
have caused these symptoms — it might have caused more 
weight to be given to the alleged sudden onset of the right 
hemiplegia. Instead of this being regarded as compatible 
with a growth, it might have been considered to be strongly 
suggestive of vascular disease. The second fact is that pro- 
gressive symptoms of local organic disease, uninfluenced by 
17 



194 INEVITABLE FAILURE. 

treatment, persisting and increasing in spite of it, may be a 
secondary effect of arterial disease. This also is not part 
of our common knowledge. The conditions which led to it 
here are, of course, most unusual, but the same result may 
be met with under conditions less exceptional. The recog- 
nition of this fact might have caused more weight to have 
been placed on the absence of the optic neuritis, which, as I 
have said, usually attends a growth of such rapid course. It 
is difficult to say whether these considerations would or 
should have made the existence of a growth unlikely. We 
must not be too "wise after the event," even if we strive to 
be wiser. 

There still remains the chief problem, Why did the patient 
die when it was thought that she would live? To be right 
or wrong matters little in itself; to prevent death matters 
everything. Without successful treatment, and except as 
subordinate to it, accurate diagnosis is as "thistledown 
without seed." In this case, it is true, the diagnostic error 
could have had little influence; it concerned only the special 
form of the disease; its nature was correctly recognised, and 
the misconception made no difference to the treatment that 
was right and was employed. But why did proper treatment 
fail ? The answer brings before us considerations of great 
importance. We know but little of the way in which treat- 
ment acts upon syphilitic formations, acts on them so surely, 
induces their rapid diminution in size, and their ultimate 
change into cicatricial fibrous tissue. We must infer from 
the quick reduction in size of such growths that the forma- 
tion of the softer cellular elements is arrested; that they 
undergo a process of disintegration, and the products of this 
quickly pass away. Those elements that are changing to 
fibres, or are actually such, are apparently incapable of such 
destruction. They seem to persist, but to shrink and con- 
tract, a change which goes on, as we see in every cicatricial 



MECHANISM OF SYMPTOMS. 195 

process, so that the uhimate result of a gumma is a firm 
nodule of fibrous tissue, such as may sometimes be met 
with in the fiver. Note that the contraction of the fibroid 
elements is, and must be, an essential part of the process. 

Such disease of the larger cerebral arteries is generally on 
the side of the wall only; it does not surround the vessel. 
Its disappearance under treatment is therefore only attended 
with a fibroid change on one side of the wall, unimportant 
unless a branch arises there which may be closed, or unless 
the substitution of extensible tissue for the elastic and con- 
tractile elements of the wall permits aneurysmal dilatation 
to take place. The ultimate condition caused by such dis- 
ease, even with effective treatment, is one great cause of 
intracranial aneurysm. But, on the other hand, if the dis- 
ease entirely surrounds the artery, the effect of the contrac- 
tion of its tissue must be to lessen the calibre of the vessel. 
This is an inevitable result, serious in proportion to the 
degree of disease, to the degree to which the wall is thick- 
ened. Fortunately such a condition is rare — it is rare for 
such disease to surround a vessel — but you have a striking 
example of it in these arteries. The growth entirely encir- 
cles each middle cerebral artery and each anterior cerebral; 
the thickening of the wall is such as apparently to obliterate 
the cavity of the vessel. On each side — on the left against 
the old thrombus, on the right where the recent clot com- 
menced — the vessel seems to be closed. In neither can we 
discern any persistent channel. There must have been one 
until the final occlusion occurred, but the opening must have 
been very small. We have here evidence which seems irre- 
sistible that the process which treatment was intended to 
induce — the process by which the morbid process lessens 
and ultimately cicatrises — could not hinder, and perhaps 
promoted, the contraction of the tissue in the wall of the 
vessel, so as to diminish the reduced calibre arteries, and on 



ig6 INEVITABLE FAILURE. 

the right side to induce the formation of the clot which was 
the cause of death. This is a starthng fact, but from it I see 
no escape. Another indication of the process of contraction 
is afforded by the sHght degree of external prominence of 
the disease in the larger arteries. Such disease, untreated, 
always projects considerably from the wall of the vessel. The 
absence of this prominence we must ascribe to the contrac- 
tion induced by the month's treatment. Contraction of 
growth in the wall of a tube lessens the external projection, 
but at the expense of the cavity. Thus we are confronted 
by the fact that, with disease of this character, so extreme 
and so placed, the treatment by which it was hoped that 
life would be saved, and health restored, could not avert, 
if it did not accelerate, the gravest consequences of the dis- 
ease. 

It is difficult to arrive at any other conclusion than that 
death in this case was inevitable. The opportunity for 
effective treatment had passed before the patient came here. 
We cannot doubt that if she had sought medical help in the 
early stage of the malady, and had received that which was 
wise and adequate, her life would have been saved. We 
must, however, remember that in patients of her sex it is 
often difficult to discern or even suspect the specific nature 
of such disease. Sometimes it is scarcely possible for any 
suspicion of this cause to arise. Not long ago I saw a patient 
in whom a morbid process of this nature seemed quite out of 
the question, and to no one was it more inconceivable than to 
a doctor who had known her from childhood. She had 
certain spinal symptoms, chiefly in the arms, which seemed 
only to be accounted for by an increase in syringomyelia or 
"central gliomatosis," such as sometimes occurs soon after 
adult life is reached. But a very unexpected revelation dis- 
closed to me the possibility of the constitutional influence 
we are discussing, and made it possible, and even probable. 



DIAGNOSTIC DIFFICULTY. 197 

that the symptoms were due to cervical pachymeningitis. 
The saying that "knowledge is power" received a perfect 
illustration, for the treatment which the knowledge entailed 
resulted in the complete removal of the symptoms, and they 
were of most threatening gravity. 

The case was an illustration of another fact of which we 
are sometimes apt to lose sight : the absolute difference which 
exists between the improbable and the impossible. Of course 
there are degrees of probability and improbability. The ex- 
tremely improbable is very near the impossible ; the two may 
seem almost alike and appear to be on the same level when we 
look along the surface of things; but between them a deep 
gulf is fixed, a gulf unbridged. The impossible cannot be; 
the improbable, however unlikely, may be. In the course 
of life you may meet with cases in which it will be useful to 
remember this. 

But I would have you, when you look at these arteries, to 
ask yourselves, What can be anticipated in such a condition ? 
You will perceive from them, more forcibly than from words, 
that no therapeutic measures can alter the clot which has 
formed in the diseased vessels. A clot in a vessel is one of 
the most stable, most enduring, of morbid states. When 
thus closed, the cavity of an artery cannot be restored, nor 
can the effects of its closure on the brain substance be pre- 
vented or materially lessened. The symptoms of such 
closure, indeed, do commonly lessen, as do those which are 
produced by the emboHc closure of an artery; they diminish 
because they are at first more extensive than correspond to 
the actual destruction of brain tissue. If iodide is given the 
improvement may be, and often is, ascribed to its influence, 
although without adequate ground.* By suitable means 
we may support and steady the circulation, and probably 

* See the preceding lecture. 



198 INEVITABLE FAILURE. 

increase such collateral supply of blood as may be possible, 
but the utmost we can effect is very little. 

Yet you should give iodide, unquestionably. The abso- 
lute necessity for treatment should be clear to you when you 
look at these vessels. Consider the wide extent of the iso- 
lated areas of disease, on the posterior cerebrals as well as 
the other vessels; hardly one is free. The disease which 
exists is always more extensive than corresponds to its ob- 
trusive effects. Symptoms seldom bring us face to face \sdth 
disease of the kind until an artery, or at least a branch of 
some importance, has been closed by thrombosis. The 
eft'ects of this we cannot change by treatment, but we can 
never tell how much more disease there may be, disease we 
can remove, nor can we tell how near such disease may be to 
the closure of a branch or trunk. Such possible effects we 
may prevent by prompt measures, and I have seen cases in 
which such treatment seemed clearly to prevent the gravest 
results. Yet treatment has to be carefully adjusted to the 
patient's state. In this case the mercury had to be discon- 
tinued on account of weakness, and the fear of further en- 
feebling her heart. It was wise, and even wiser than was 
then discerned, because the risk of a fresh thrombosis was 
more imminent than could be perceived. On account of 
this danger it is not well to give, in such cases, the very large 
doses of iodide of potassium that are sometimes employed. 
Iodide is credited, as you know, and I think with reason, 
with the power of promoting coagulation of the blood, and 
has been employed for this purpose in aneurysm. Hence 
very large doses may facilitate the formation of a clot in a 
narrowed vessel. The dose which the patient had — 15 grs. 
three times a day — is large enough, as I have many times 
seen, to influence such disease as rapidly as is reasonably 
possible, if the patient has not already been taking it, and is 
as much as it is wise to give under the circumstances. 



CONCLUSION. 199 

Let me end by looking back at our starting place. This 
was the fact that we sometimes fail to save life when we 
expect to succeed, even when we have reason for our expec- 
tation. Such failure is among the sources of the distress 
which the incidents of our work so often cause, especially to 
young practitioners. But the facts of the case we have con- 
sidered should fix in your mind the truth that even the full 
knowledge, which so seldom is within reach in ordinary 
practice, may demonstrate that the failure was inevitable, 
that the end could not have been averted by any means we 
could have used, or delayed by any effort we could have 
made. Thus it was here, and the same is often true when it 
cannot be ascertained. Therefore, do not let the discrepancy 
between your early forecast and the later fact, cause you to 
give way to misgivings which may be groundless, and regrets 
that must be vain. 



LECTURE VIII. 

SYRINGAL HEMORRHAGE INTO THE 
SPINAL CORD.* 

Delivered at the National Hospital for the Paralysed and Epileptic, 
February 8, 1903. 



The human frame is the most complex and elaborate 
structure known to us. It is not surprising, therefore, that 
its development should sometimes fail to achieve comple- 
tion, or that this failure should occur in the most elaborate 
of all its parts, the central nervous system. Defective de- 
velopment is found most frequently in the spinal cord, and 
it is to one effect of this imperfection that I ask your atten- 
tion to-day. The precise defect we are concerned with is 
that which entails the presence of pecuhar cavities in the 
cord. Such cavities have been ascribed in some cases to 
other causes. To this I will refer presently, but it is certain 
that they are often, and perhaps generally, the result of a 
local arrest of the process of development. 

You know that the spinal cord is, at one stage, an elon- 
gated mass of embryonal tissue, having a medial furrow, 
the sides of which ultimately close. You know that the 
closure may fail to occur in part, and that even the closure 
of the bony canal may not take place, with "spina bifida" 
as the result. You know — I hope that I am not presuming 
on too much knowledge — that the defect in the bony canal 
may be sHght or even absent, and yet it may be definite in the 

* Lancet, October 10, 1903. 
200 



SYRINGO-MYELIA. 201 

spinal cord. You may also know that there may be defec- 
tive development within the parts that do coalesce. Em- 
bryonal tissue persists where its development into nerve 
structure fails to occur, and often there is an actual cavity 
in this tissue. Thus we may have cavities where closure 
has failed to occur, with or without adjacent embryonal - 
tissue, or we may have cavities where persisting embryonal 
tissue has broken down. Those are the essential facts of 
what is called "syringo-myelia." There may be a cavity 
in the middle line, usually continuous with the central canal, 
where should be the posterior medial raphe. This is obvi- 
ously due to imperfect closure. Or there may be a cavity 
adjacent to the posterior horn, often one on each side, but 
unequal in extent. These may be continuous with the cen- 
tral canal on one side or on both. 

These lateral fissures in the posterior columns are espe- 
cially important from a pathological point of view. In the 
process of normal development, a portion of embryonal 
tissue becomes isolated, and remains, unchanged, as the 
gelatinous "caput cornu posterioris." The lateral cavities 
apparently result from an abnormality or imperfection in 
this process. All the developmental cavities occur in the 
posterior and central regions of the cord, — a fact that is in- 
telhgible, since this region is the last to attain structural com- 
pleteness. But such cavities, when dilated, may compress 
and damage the anterior horns, with muscular atrophy as 
the result, and even the lateral columns of the cord, causing 
spastic paralysis of the legs. 

It has been maintained of late that similar cavities in 
the spinal cord sometimes result from preceding haemor- 
rhage, and Schultze* has suggested that their origin may 



* Zeitschrift f. Nervenk., 1902. See also A. Westphal, Arch. f. Psych., 
1903. 

18 



202 SYRINGAL HEMORRHAGE. 

be minute haemorrhages in the grey matter caused by diffi- 
cult birth. This is a possible cause, although not yet proved. 
But their precise origin does not concern us now. It is their 
presence and not their cause with which we have to do. 

The developmental nature of these cavities is often sug- 
gested by the fact I have mentioned — that they are bordered 
by undeveloped embryonal tissue. It forms a bounding layer, 
sometimes encroached on by erosion when liquid has long 
distended the cavity, sometimes considerably increased by a 
process of growth. Such residual tissue is prone to increase 
and its growth is occasionally so considerable as to constitute 
what is called "gliomatosis," i. e., a glioma which can be 
traced to exuberant morbid development of such residual 
tissue. The word gliosis has been applied to it when it does 
not form a distinct tumour. The normal neuroglia is the 
remains of this embryonal tissue, and gliomata elsewhere 
have been thought to arise from spots of such residual tissue. 
It is certain that glioma of the pons — that infiltrating growth 
which causes great enlargement before it interferes with 
function — is sometimes connected by tracts of similar tissue 
with gliosis around a congenital cavity in the cervical spinal 
cord. This is a pregnant fact. It supports the hypothesis 
that such tumours may have their origin in residual unde- 
veloped embryonal tissue. It shows us also that these 
developmental defects may extend up from the cord to the 
mesencephalon, although they seldom pass up as actual 
cavities. We shall presently see the importance of this fact. 

The symptoms produced by this variable state arise, as 
I have said, in consequence of the distension of the cavities 
or the growth of the adjacent tissue. Indeed, some may be 
due to the absence of the nerve tissue which has not formed. 
The former generally come on after adult life is reached, 
but those which are due to simple defect exist from birth. 
You know the common characteristic of those of the first 



SYRINGO-MYELIA. 203 

class — pain, analgesia without anaesthesia, and muscular 
wasting when the anterior grey substance in damaged. But 
the symptoms vary in different cases, just as do the cavities, 
* and they are sometimes such as would not suggest their 
cause. Indeed, such cavities are sometimes found when 
no symptoms can be heard of, and we should therefore be 
prepared for the fact that the symptoms may often be slight, 
and not characteristic. With unsuggestive symptoms, we 
can hardly suspect this cause unless there is the additional 
evidence of imperfect development afforded by defective 
closure of the spinal bones, called ''spina bifida occulta." 
Such imperfect closure of the bony canal, with no external 
tumour, affords ground for suspecting a like state of imper- 
fection in the spinal cord. 

Let me tell you of a case in which this evidence was most 
suggestive. A man, thirty-five years of age, had suffered 
much pain in the arms for eight years. He was a profes- 
sional musician. Use of the arms in playing relieved the 
pain for a time and then increased it; the use induced also 
a feeling of powerlessness. When I saw him the pain ex- 
tended down the inner side of each arm, and was especially 
great in the upper part. Objectively, nothing abnormal 
could be found. There was no tenderness and no deficient 
sensibility of any kind. The only thing discovered was 
that the right trapezius was a httle smaller than the left, 
and presented distinctly less excitabihty and contraction to 
both faradism and voltaism in all its parts. 

The case had baffled the doctors who had seen it; by one 
it was regarded as myelitis. The key to what I believe was 
its nature was this fact. At the bottom of the dorsal spine 
was a peculiar cicatrix, something like the umbilicus, but 
with furrows running from it a short distance to right and 
left. On this were a few large hairs, a very suspicious indi- 
cation. The first two lumbar spines could not be felt; they 



204 



SYRINGAL HEMORRHAGE. 




Fig. 14. — Position of cicatrix on back. 




Fig. 15. — Cicatrix, natural size. The large hairs upon it can be clearly 

seen. 



SYRINGO-MYELIA. 205 

were apparently absent. The scar had been there as long 
as he could remember, and he had been told that it was 
present at birth. If so, it seemed to be a case in which an 
external spina bifida had sloughed away in utero. At any 
rate it was clearly a case of ''spina bifida occulta." This 
involved a high probabihty, almost certainty, of a defective 
spinal cord in that region, and we know how often this is 
associated with imperfect development higher up, with a 
fissure or fissures. The fact made syringo-myelia the prob- 
able cause of the pain, and we could thus understand why 
no treatment had had any influence on his sufferings. If 
the assumed nature of the case is correct, it is an illustration 
of the various and dubious symptoms which may be pro- 
duced by such congenital disease. 

But it is not with these cases, with trifling symptoms, that 
I am specially concerned to-day. I wish to direct your 
attention to some evidence that the existence of these cavi- 
ties occasionally induces the occurrence of one of the gravest 
lesions of the spinal cord, hemorrhage, and determines spe- 
cial, perhaps characteristic, symptoms. I have seen several 
cases in which the peculiar character of the symptoms can 
be best understood by ascribing them to a haemorrhage into 
such a cavity as we have considered. In some cases, other 
symptoms made this probable. 

First, however, let me give you a fact which proves that 
this is not a purely hypothetical pathology. I show you 
sections from a spinal cord in which such syringal haemor- 
rhage had occurred. A series of the sections are figured in 
my "Manual of Diseases of the Nervous System" (Vol. I). 
A cavity passed from the position of the central canal back- 
wards and outwards, along the left posterior horn, and 
extended from the cervical region to the lower part of the 
cord. Through part of the dorsal region there was a simi- 



2o6 SYRINGAL TLEMORRHAGE. 

lar small cavity on the right side. That on the left was 
distended with blood throughout. Haemorrhage into it had 
apparently commenced in the cervical region, for here the 
cord was so broken up by extravasation that only a layer of 
nerve tissue remained outside the blood. It is probable that 
the blood had escaped into the cavity in this part, and had 
gravitated downwards, after distending the whole cavity; the 
resistance caused the blood to work its way into the spinal 
cord at the seat of the primary haemorrhage, and to cause 
death, partly by the local destruction it wrought and partly 
by the adjacent inflammation it excited, which ascended 
the cervical enlargement until all the muscles for breathing 
were rendered powerless. 

The case occurred here twenty-five years ago, and the 
notes are imperfect, but they show certain important facts. 
The patient was a coachman forty-eight years of age, and, 
as far as could be learned, he had had no preceding symp- 
toms to suggest the existence of these cavities. The onset 
was acute, but not instantaneous. One evening, at his 
work, he found his legs "giving way," but managed to walk 
home. The next morning he could not stand, and in the 
course of the day he ceased to be able to move his legs. He 
did not lose all power of contracting the muscles; this indeed 
persisted even to the end of life, nearly five weeks after the on- 
set. Such a development of symptoms, acute, but not sudden, 
suggests myehtis, and so do the facts that the man was not 
temperate, and had lately been much exposed to cold and wet. 
But there were other symptoms which indicated more than 
inflammation. During the first night he had most painful 
tingling between the knees and ankles, and this was followed 
by pain behind the knees, and very intense pain in the spine. 
Even when admitted to the Hospital three weeks later, any 
movement of the body caused pain in the spine, "as if a 
knife were driven down it," pain that made him shriek. It 



SY^IPTOMS. 207 

was attended by severe but less sharp pain in the legs, "as 
if they were being broken across." Such pain does not 
occur in simple myelitis; it is commonly a result of haemor- 
rhage. When admitted, three weeks after the onset, he had 
lessened sensibility to touch over the legs, but that to pain 
and to heat was increased, — a strange condition, hardly 
known in myelitis. There was flaccid palsy, with loss of all 
reflex action. Weakness of the arms developed during the 
fourth week of the disease, and became complete at the 
shoulders and elbows, but some movement of the fingers 
continued to the end. With this loss, movement of the 
thorax failed on the left side (that of the syringal haemor- 
rhage) earlier than on the right, and was followed by paral- 
ysis of the diaphragm and difficulty in swallowing. During 
the last days of life occasional contraction of the sterno- 
mastoid and extra-respiratory muscles alone efl'ected some 
sKght breathing, insufficient to maintain life. He died on the 
thirty-third day from the onset. Almost to the last he could 
feebly contract most of the muscles of his legs, and those 
moving the hands. 

I have told you the lesion that was found, extravasation 
into a cavity beside the left posterior horn, extending from 
the cervical region downwards. From the chief seat of 
haemorrhage some blood had escaped outside the cord. 
There was no upward haemorrhage within the cord, but there 
were signs of ascending myelitis, and to this secondary in- 
flammation we must ascribe the latter fatal ascending paral- 
ysis. The precise relation of the sequence of symptoms to 
the morbid process is not easy to discern, but some important 
points are distinct. One fact the case illustrates is that the 
onset of the symptoms of syringal haemorrhage may be less 
sudden than those of haemorrhage usually are. If the blood 
escapes into a cavity of considerable vertical extent, there is 
not much erosion of the cord at the seat of the haemor- 



2o8 SYRINGAL HEMORRHAGE. 

rhage until the cavity is filled. In this case it is probable 
that such erosion did not occur until after the haemorrhage 
into the cavity had ceased, and that a renewal of haemorrhage 
was excited by the removal of the patient to the Hospital, 
and this invaded the substance of the cord at the place of 
least resistance. In the second place the effect of such 
haemorrhage on the function of the cord may be less absolute 
and less consistent than those produced by a primary ex- 
travasation into its substance. Thirdly, the case shows how 
the effect of such a lesion may be increased by secondary 
myelitis, a slower subsequent process, the danger of which 
should always be remembered. 

I have mentioned that the opinion has been maintained by 
some authorities who have given much attention to the sub- 
ject, that many cavities regarded as congenital are not such, 
but are the result of haemorrhage. But the case I have related 
shows what care is necessary in concluding that a circum- 
scribed space occupied by blood through a considerable 
extent of the cord, was produced by the extravasation found 
in it. It might have been thought that, in this case, the 
haemorrhage had forced its way down the cord and thus 
caused the cavity it occupied, were it not for the definite wall 
the cavity possessed and for the symmetrical fissure on the 
other side, adjacent to the right posterior horn. It was not 
continuous with the other, and contained no blood, but the 
symmetry leaves no doubt of their congenital nature. Were 
it not for this second fissure, it would have been easy to think 
that the other was actually produced by the fatal haemor- 
rhage. 

We can understand that haemorrhage may easily occur 
into these pre-existing cavities. They are irregular in posi- 
tion and in size, and therefore in their relation to vessels. 
The adjacent ghomatous tissue, the residual embryonal 
tissue which surrounds them, seems to be readily broken 



SYMPTOMS. 209 

down by the fluid they contain. Adjacent vessels are im- 
perfectly supported, and may easily givT way. Moreover 
the gliomatous growth which occurs is vascular and may be 
a source of haemorrhage. In a case recently described by 
Dr. Alexander Bruce,* fatal haemorrhage had occurred into 
a gliomatous tumour in the cord, containing cavities. The 
tumour was apparently due to local growth of residual tissue, 
but it was so vascular as to deserve the name " angio-glioma." 
The extent of the resulting extravasation will depend upon 
the size of the vessel, and, if the blood escapes into a cavity, 
on the vertical extent of this. Lastly, the symptoms pro- 
duced will vary according to the force with which the blood 
flows out, and to the secondary effect of the haemorrhage. 
It is important to remember that haemorrhage may produce its 
manifestations by destruction of tissue, by pressure, by slower 
erosion of the adjacent structures, and also by secondary 
inflammation, such as always results from a traumatic pro- 
cess. Thus, some effects of the condition may not coincide 
with the primary extravasation, but may be developed as 
this increases, or they may more slowly follow^ it. 

Let me now mention to you the symptoms of two cases 
which are, I think, only to be explained by assuming that 
haemorrhage occurred into such a pre-existing cavity. It 
is perhaps significant that the diagnosis has to be a matter 
of inference and not of demonstration. It signifies that 
haemorrhage confined to such cavities is a less fatal lesion 
than haemorrhage into the substance of the cord. As we 
have just seen from the case I have mentioned, the latter 
may be a secondary effect; haemorrhage into a cavity may 
escape beyond it, may work into the substance of the cord, 
as in the case I have mentioned, with far graver eft'ects than 

* Scottish Med. and Surg. Journ., Aug., 1902. 



210 SYRINGAL HEMORRHAGE. 

if the extravasation is limited to the cavity, as we may assume 
it was in the cases I have to describe. They differ widely in 
their symptoms, but they agree in two features, in the promi- 
nence of sensory loss, and in its peculiar seat and limitation, 
while the first case presents a distribution of motor palsy 
which it is scarcely possible to explain, except on the suppo- 
sition I have advanced. In considering the symptoms, re- 
member that the cavities occur chiefly in the posterior region ; 
hence we can understand the degree of sensory impairment. 
Remember also that a cavity along the posterior cornu if 
distended by blood, may compress the lateral column, and 
if it extends forward to the central region, it may compress 
the anterior horn. Remember, lastly, that such haemorrhage 
is very slowly absorbed; ultimately the extravasation lessens 
in bulk, as the disintegrated blood is removed, and thus 
symptoms due to compression and not to destructive lacera- 
tion may ultimately pass away to an extent that would not 
be expected from their initial degree, and would scarcely be 
thought possible from the long time during which their sever- 
ity is maintained. This seems to be the lesson of the first 
case, and, if it can be trusted, it shows how important it is to 
recognise the morbid process. It will justify hope, when 
otherwise there would only be despair. 

Case i. — ^A member of our own profession. Dr. C, forty 
years of age, after a good deal of worry and a hard day's 
work in very cold weather, felt at night a momentary stab 
of pain in the right side of the head, followed by a pecuhar 
sense of giddiness, objective vertigo in the dark. Although 
he could see nothing, he felt as if everything before him were 
passing from one side to the other. Then he fell asleep. At 
three o'clock he woke up to find his arm powerless. He 
pinched it and discovered that it was also insensitive. Next 
morning it was found to be completely paralysed, without 



SYMPTOMS. iit 

movement and feeling, and so it remained. The condition 
was just the same when I saw him three months later. Even 
at first there was no weakness of the face or of the leg. Sud- 
den paralysis of the left arm, preceded by sudden pain in the 
right side of the head and giddiness, naturally suggested a 
cerebral lesion, and it was thought by the doctors who saw 
him that there had been thrombosis of a cortical vessel on 
the right side of the brain. Such sudden palsy always indi- 
cates a vascular lesion, rupture or closure. But there was no 
heart disease to indicate a source for embolism, and cerebral 
haemorrhage at forty without renal disease was most un- 
likely. 

His symptoms, when closely scrutinised, were incompat- 
ible with disease of the brain. The points of distinction 
are instructive. A cerebral lesion never causes complete 
paralysis of the arm, without any affection of the face or leg. 
The structures are in such contiguity that absolute destruc- 
tion of the centre for the arm, or the path for the arm, cannot 
occur without such implication of the adjacent regions for 
the face and leg as to cause impairment of their function, at 
any rate for a time. Moreover, in cerebral paralysis of the 
arm, the muscles of the shoulder girdle are never completely 
paralysed. In this case the affection of the muscles was 
remarkable. There was complete loss of power of the trape- 
zius, of the sterno-mastoid, and of the pectorahs on the left 
side. Movement of the head to one side may be at first 
weakened from brain disease, but complete paralysis of the 
neck muscles never occurs, and the sterno-mastoid is weak- 
ened on the side opposite to the affected arm. This peculiar 
palsy of the neck muscles proved that the condition was due to 
a lesion of the spinal cord. The affection of sensibihty con- 
firmed this in a striking way. There was complete loss of 
sensibility in the forearm below the elbow, and it was greatly 
diminished on the outer part of the upper arm and slightly 



212 SYRINGAL HEMORRHAGE. 

on the inner side. The greater loss extended over the 
shoulder and the side of the neck almost to the edge of the 
jaw, and behind almost to the occipital bone, everywhere 
ceasing suddenly. It also passed down over the thorax, 
behind to the level of the angle of the scapula, and in front 
almost to the edge of the ribs, everywhere stopping at the 
middle line. On the face, head and abdomen, sensation 
was normal. Such a distribution could not result from cere- 
bral disease. From this cause the loss which extended up 
the neck would certainly have passed on to the face and head, 
and also from the thorax to the abdomen. Thus, this also 
clearly indicated a lesion of the spinal cord. The suggestive- 
ness of the pain in the right side of the head was lessened by 
the fact that he had been liable to such pain for some years. 
Transient vertigo has Httle locahsing significance, and, as we 
shall see, it could be otherwise explained. 

The mystery of a spinal lesion so severe, and yet so limited 
in effect, damaging the left side of the cord so gravely and 
yet not interfering with the right side, would have been very 
great but for another symptom, which suggested an explana- 
tion for its occurrence and also for its limitation. He had a 
congenital defect of certain movements of the eyes. They 
were habitually directed to the left, and could not be moved 
at all to the right of the middle hne. Indeed the left eye 
was habitually directed outwards mid- way to the outer can- 
thus and could not be brought even up to the mid-position, 
nor could it be moved outwards beyond its habitual position. 
Yet it could be moved obliquely downwards and outwards. 
It could not be moved upwards, and with this was associated 
a Httle drooping of the lid. The right eye could be moved 
inwards, upwards and downwards well, but not outwards at 
all. Thus there was a congenital absence of movement of 
both eyes to the right, and of almost all movement of the left 
eye. Such a condition, hfe-long, means a congenital defect 



SYMPTOMS. 213 

of structure in the upper part of the pons on the left side. 
We know that such defects in the pons may be associated 
with similar defects in the spinal cord, and that in the cord 
these take the form of syringomyelic cavities or fissures, 
usually, as I have said, with an adjacent layer of gliomatous 
tissue and often with separate tracts of such tissue. Thus, 
the condition of the eyes revealed the probabihty of a state 
of the cord such as might have determined both the occur- 
rence and the limitation of the disease, a congenital cavity 
into which the haemorrhage had occurred. A congenital 
associated defect in the pons would fully explain the peculiar 
vertigo, since a sudden hemorrhage into the cord might 
cause disturbance of the equihbrial centre in that part, espe- 
cially if the two conditions were structurally connected. 

Three months later the loss of sensation had lessened in 
degree; it still extended over the same regions, although at 
the margins it passed more gradually into the normal state. 
The paralysis remained as before; although he could just 
contract the trapezius and sterno-mastoid, he could not con- 
tract the pectoralis. All the muscles had wasted, but only 
in a moderate degree, and, as at first, there was merely a 
diminution in electrical irritability, just the same to faradism 
and to voltaism. We can understand this if the anterior 
grey matter was compressed by the haemorrhage but not 
destroyed. It would be so compressed if a cavity beside the 
posterior horn extended forwards to the neighbourhood of 
the central canal. The wrist-jerk was increased and there 
was some excess of knee-jerk, but without weakness of the 
leg. 

I have not seen Dr. C. since, but I have lately learned that 
after two years the power gradually began to return, and 
that he has since regained fair poAver over all parts of the 
arm. I am glad to say that absolute confirmation of the 
diagnosis is still lacking, for he is otherwise in excellent 



214 SYRINGAL HEMORRHAGE. 

health. But there has not been wanting some evidence of 
the accuracy of the diagnosis. You perhaps know that the 
pecuhar joint disease met with in tabes, with enlargement of 
the ends of the bones, is also met with in syringomyelia. 
This patient, after the attack of paralysis, had increasing 
trouble at the hip-joint. He believed that at two years of 
age the joint had been dislocated and the displacement re- 
duced, but such an accident would manifestly not explain 
grave and increasing trouble after mid-life. Mr. Symonds 
took him into Guy's Hospital and operated. He found the 
head of the femur enlarged to twice its natural size, and he 
sawed it off. The edges of the acetabulum were thickened 
to twice the normal. The patient made a good recovery and 
has since acquired a most useful new joint. 

The condition presented so close a resemblance to this 
special arthropathy as to constitute some corroboration of 
the diagnosis of syringomyelia, in spite of the absence of any 
change in the sensation in the leg. As I have said, the great 
cause of tabes (syphiHs) could be quite excluded. But an- 
other peculiar symptom occurred, which may be taken for 
what it is worth. It is said that "phlebitis," i. e., venous 
thrombosis, is more common in the subjects of syringomyelia 
than in others. Whatever may be the value of the assertion, 
this patient had a clot in some veins of the leg on two occa- 
sions, first soon after the attack of paralysis, and again after 
the operation. All things considered, I think we have reason 
to believe that there occurred, in this case, haemorrhage into 
a syringal cavity and that the evidence is as strong as we can 
expect to meet with, short of pathological proof. 

Case 2. — In the next case, also, evidence of a similar lesion 
is such as to amount to an equally high probability. It is 
that of a man, the subject of the haemorrhagic diathesis. 
From this, the sons of his sisters also suffered, although the 



SYMPTOMS. 215 

sisters themselves escaped — a peculiarity met with in some 
other congenital diseases, notably in pseudo-hypertrophic 
paralysis. At the age of sixteen he gave himself a sudden 
shock by jumping over a box; he felt Httle immediate effect, 
but the next morning had lost power and sensation in the 
legs. He slowly recovered fair power of movement, but 
considerable defect of sensibihty remained, and was present 
when I saw him, twenty years after the onset. During the 
intervening time he had some attacks of transient swelling of 
the knee-joints, thought to be due to haemorrhage into them, 
such as occurs in the subjects of this diathesis. Some defect 
of power of flexing the ankles was the only motor symptom 
that continued. He had suffered for years from pains in the 
legs, intermittent at first, but lately more constant, and he 
had a troublesome ulcer on one toe, which was obstinate, and 
when healed was prone to break out again. But the loss of 
sensibihty persisted, and was unchanged when I saw him. 
It was complete to both touch and pain, and was remarkable 
in its distribution. It extended over the lower and inner 
half of each buttock, down the middle of the back of each 
thigh, the outer part of each leg, and over the feet, — soles 
and heels, but sparing the inner side, and a small area on the 
outer side of the left foot had escaped, where there was some 
hyperaesthesia. With the exception of this hyperaesthetic 
area, the loss was perfectly symmetrical, and corresponded 
precisely to the sensory distribution of the last (fifth) lumbar 
and all the sacral segments of the spinal cord, the distribu- 
tion of the fourth lumbar escaping entirely, even on the inner 
side of the lower legs and feet. Such a correspondence to 
structural arrangement is most unusual in a lesion of the 
cord such as inflammation or common haemorrhage; the 
lesion and its eft'ects have then a random distribution. The 
peculiar seat can only be explained by assuming a struc- 
tural condition which determined the effects of the disease. 



2i6 SYRINGAL HEMORRHAGE. 

The only condition we know that will explain it is a con- 
genital cavity or cavities, central, and extending back in the 
medial line, or bilateral and symmetrical in the posterior 
columns, conditions which, as we have seen, are occasionally 
met with. It is easy to understand that the haemorrhagic 
diathesis might have caused slow bleeding into such a cavity 
as the result of the concussion, and a trifling difference in 
the extent or position of the cavity on each side might have 
led to the escape of the hyperassthetic area on the left foot. 
From what we know of the bleeding in this constitutional 
condition it is easy to understand that it should have occurred 
slowly, from a very trifling source, and that thus its effects 
only became manifest the morning after the concussion. 
The case agrees with the last, and indeed exceeds it, in the 
pronounced and persistent character of the sensory loss. 
Moreover, it agrees also in the presence of another corrob- 
orative condition. Joint changes were present here also. 
There was thickening of the ends of the bones forming the 
knee-joint, quite like that of tabetic arthropathy, and there 
were also chronic changes in the hip-joints. Extension of 
both the knee- and hip- joints was limited by the arthritic 
changes. 

Case 3. — I may mention a third case, which was possibly 
of the same nature, although the symptoms were less definite. 
A girl, aged twenty-one, was admitted here with paraplegia 
of two months' duration. For eighteen months the left leg 
had occasionally given way for a moment, lately more often, 
and slight weakness had developed. This sudden transient 
"giving way" of the legs is often regarded as evidence of hys- 
teria, especially if met with in a girl. It is often, however, 
a forerunner of organic disease. During the month before 
the onset of severe palsy, the right leg had shared the weak- 
ness of the left, and there had been troublesome cramp-like 



SYMPTOMS. 217 

pains in the feet. Seven weeks before admission complete 
paraplegia came on very rapidly. The legs one day were 
much weaker, and the next were completely paralysed in 
motion and sensation, with much pain in the left leg, and 
for a day or so acute pain in the spine. A pain around 
the abdomen at the level of the umbiHcus was felt for a few 
hours from time to time. On admission, the ankles could 
be slightly flexed and all the intrinsic muscles of the feet 
could be contracted. The calf muscles were powerless, and 
so were those of the knee- and hip-joints. The knee-jerks 
were lost, and there was no plantar, abdominal, or gluteal 
reflex. No faradic irritabihty could be elicited in the 
glutei, the flexors of the knee, or the calf muscles, but it 
remained in the extensors of the knee, better on the right 
side, and it was present also in the peronei and tibialis 
anticus of the left leg. Voltaism seemed to be lessened in 
the same way as faradism. The muscles were not much 
wasted, and I may anticipate by saying that during her 
stay in the hospital (four months) the muscles gradually 
recovered, and all regained good faradic irritabihty. Their 
perfect recovery thus makes it improbable that there had 
been a primary lesion of the anterior horns, such as acute 
poliomyelitis, a fact which renders the sensory condition 
more important. 

Sensation to touch was lost over both legs, except on the 
inner side of the right leg above the ankle, but it was abso- 
lutely lost on the corresponding region of the left. It was 
lost on both soles, including the heels, and this loss extended 
over the outer half of the dorsum of each foot. But this 
plantar loss on the left foot spared the last phalanges of 
the toes, while on the right foot only those of the great and 
little toes had escaped. On the lower legs, loss was not 
quite absolute below but became so about three inches from 
the knee, and this continued up the back of the thighs and 
19 



2i8 SYRINGAL HEMORRHAGE. 

over the gluteal region to the crest of the iliac bone, where 
it was succeeded by a zone of hyperassthesia, extending up 
to the ribs. It was absolute also on the front of the thighs 
and lower part of the abdomen, in the hypogastric and 
inguinal regions, becoming less in the umbilical region, but 
only normal near the ensiform cartilage. The alteration to 
pain corresponded in general with that to touch, but on the 
soles, where touch was lost, pain was only delayed, and so 
also on the back of the left foot. There was the same in- 
creased sensitiveness to pain as to touch on the back, above 
the iliac crest. 

A month after admission she could perform all move- 
ments of the legs, but sensation was almost the same. It 
slowly improved, by general diminution rather than by local 
change. When she left the hospital there was only absolute 
loss in the hypogastric region and on a spot on the outer 
side of the right foot, and on the inner side of the left leg. 
The knee-jerks were still absent; the legs could be moved 
freely and with force in any way as she lay, but it was im- 
possible for her to stand on account of the extreme degree 
of incoordination. 

I think that this case may possibly have been syringal 
haemorrhage. It is certainly one of disease causing exten- 
sive abohtion of the functions of the lower part of the cord, 
and the predominant change in sensation, its persistent 
character, the enduring loss of the knee-jerk, and the ex- 
treme residual incoordination, all indicate damage to the 
posterior columns, apparently interfering with the posterior 
nerve roots before they reach the grey substance. The 
degree and general symmetry of this damage suggest haemor- 
rhage into a cavity or cavities. 

I have seen some other cases which I think may be of the 
same nature, but they are not sufficiently pointed in their 
indication or precise in their record to make it worth while 
to take up your time with their details. Those which I 



PATHOLOGY. 219 

have mentioned are sufficiently suggestive to warrant the 
pathological conception of haemorrhage into pre-existing 
cavities, "syringal haemorrhage." As I have said, we may 
reasonably assume that extravasation may occur into any 
cavity, irrespective of its origin. The vascularity of adjacent 
gliomatous tissue, especially when this takes on a process 
of growth, is often great. It is intelhgible that these should 
sometimes give rise to haemorrhage, and it is therefore not 
surprising that such growths should sometimes contain the 
remains of small old extravasations. Little significance can 
be ascribed to these as regards the original causation of the 
cavities with which the condition is associated. I refer to 
this incidentally. My chief object is to call attention to 
the class of symptoms which seem to indicate haemorrhage 
into the cavities. I hope that further similar facts may be 
ascertained. For actual confirmation we may have to wait. 
As I have said, purely syringal haemorrhage seems to be 
seldom fatal and the fact makes the diagnostic question of 
great importance. Death seems generally the result of the 
eroding extension of the extravasation into the substance of 
the cord, or a later result of secondary spreading inflamma- 
tion, which is so grave when excited by an irritant cause 
such as haemorrhage. 

If any therapeutic lesson is to be obtained from the cases 
I have described, it is the extreme importance of rest, perfect 
and prolonged, in every case of sudden spinal palsy, espe- 
cially when pain suggests a haemorrhagic cause. If removal 
to a hospital is necessary, the patient should be completely 
passive. The slightest effort on his part to assist may 
increase the haemorrhage, or start afresh that which had 
ceased. Moreover, not only should everything be avoided 
that may increase the blood pressure in the spinal cord, but 
an endeavor should be made to lessen that which gravita- 
tion tends to cause. If possible, the position should be 
such that the spine is not the lowest part. There is a common 



2 20 SYRINGAL HEMORRHAGE. 

tendency in arranging the treatment of affections of the 
spinal cord, to consider the organ more than the process. 
In acute affections, at any rate, this is a mistake. It may 
be said, as a general rule, that in proportion to the acuteness 
of disease, the elements of treatment should be determined 
by the nature of the morbid process rather than by the 
nature of the organ affected. The importance of this is 
clear if you consider the lesion we have been discussing, 
haemorrhage. The organ into which it occurs is of shght 
importance compared with the nature of the lesion, so far 
as treatment is concerned. The object to be kept in view 
is to promote the cessation of the escape of blood, and for 
this no influence is too slight to be neglected, and the effect 
of gravitation, for good or ill, is often overlooked. In 
spinal haemorrhage, whenever it can be endured, the prone 
position of the body should be maintained; and if this is 
impossible, the patient must be kept on the side. If haemor- 
rhage occur into the leg the hmb is not allowed to hang 
down, and if it is even suspected in the spinal cord, this 
should not be the lowest part of the body, as it is when the 
patient lies on the back. Indeed, I think that, in some 
cases at least, the sitting posture, with legs depending, 
would be the most likely to promote cessation of the haemor- 
rhage, if only perfect stillness can be maintained. But 
remember the importance of posture in all acute affections. 
If you only carry away this lesson you will not have listened 
in vain, for it is one that you are sure to need in your future 
work. You may never meet with a case presenting such 
symptoms as suggest syringal haemorrhage, but you are 
sure to meet with cases of acute disease of the spinal cord. 
You will be able to understand them better, and deal with 
them more wisely, for your study of such cases as I have 
described. You cannot gain real knowledge, of any kind, 
that has not far wider applications than is at first apparent, 
or may not help you when and where you least expect. 



LECTURE IX. 

MYASTHENIA AND OPHTHALMOPLEGIA. 



The mysterious malady commonly called "myasthenia," 
or "myasthenia gravis," is a rare disease, the special charac- 
ters of which have only been discerned during recent years. 
Indeed, it is still not known, even by name, to many members 
of the profession. It is met with chiefly in the first half of 
adult hfe, and is characterized by general feebleness of the 
muscles, and also by their quick exhaustion on use, and the 
quick renewal by rest of what power they possess. The 
same feature is often, but is not always, conspicuous when 
the muscles are stimulated by electricity; the eft'ect of a 
tetanizing faradic current of given strength soon, as a rule, 
ceases, but returns after a brief rest. This weakness is not 
attended by definite wasting, or loss of electrical excitability. 
Although general, it is especially marked in the lips, palate, 
pharynx, and often in the muscles of mastication, and in 
those of the eyeball. The "bulbar" weakness, indeed, first 
attracted notice, and the condition has hence been termed 
also "myasthenia bulbaris." 

The course of the disease presents curious variations, but 
is seldom definitely progressive, nor has great improvement 



* This article is not, strictly speaking, a lecture. It was contributed to 
the special issue of the "Deutsche med. Wochenschrift, " in honour of 
the seventieth birthday of Professor v. Leyden. An English version, re- 
written, appeared in the "British Med. Journal," May 25, 1902. 

221 



222 MYASTHENIA AND OPHTHALMOPLEGIA. 

been often seen, except as a transient event. Death has been 
the result of intercurrent disease, and has yielded no clear 
indication of the nature or even the seat of the malady. In 
the absence of fact, theories have abounded. Treatment has 
seldom had marked effect. 

The symptoms vary in different cases, and in some there 
has been considerable loss of power in the eye muscles. The 
object of this paper is to describe three cases in which this 
feature was very marked, and also to call attention to another 
symptom which each presented, a peculiar alteration in the 
smile, due to the absence of the normal action of the zygo- 
matic and risorius muscles. The general features of the dis- 
ease will be perceived from the account of the cases; the 
special symptoms can be afterwards described and an attempt 
made to discern what indications they suggest regarding the 
nature of the disease. 

Case i. — This patient came under my observation long 
before myasthenia became a clinical conception. She was a 
girl of twenty-three, and was seen first in 1874, and from 
time to time during the following four years. Soon after 
this she died from some intercurrent disease. My notes 
are incomplete, but they record the chief features of the case. 

No family history of neuroses could be ascertained, no 
preceding disease, nor any exciting cause for the affection. 
Beyond a tendency to headache she had been wtII until the 
age of twenty-one, when her symptoms were first noticed; 
they commenced gradually, and slowly increased. During the 
next six months they increased shghtly, but afterwards were 
almost stationary, some indeed diminishing. The aspect of the 
patient at once attracted notice by the stiff look of the eyes, 
and the unnatural expression of the lower part of the face. 
On closer observation, it was seen that the latter depended 
on the absence of any natural smile. Instead of a move- 
ment outward of the angle of the mouth, when she smiled 



CASES. 223 

or laughed, there was only an elevation of the upper lip. 
There was no action of the zygomatics or risorius, but the 
levators raised the upper hp, causing a furrow above it beside 
the nose, and even wrinkling the skin there. Thus there 
was only an unpleasant snarl as the expression of a pleasant 
emotion. There was slight drooping of the eyelids, greater 
in the left. Movement of the eyes was much lessened. 
That of the left eye, outwards and inwards, was reduced to 
one-eighth of an inch. The right could be moved inwards 
to the full extent, but not outwards beyond the mid-position, 
to which it was brought back. Hence an attempt to con- 
verge caused an excessive movement of the right eye. Both 
moved downwards freely; upwards there was a very shght 
movement of the right eye above the mid-position, none in 
the left. The fundi were normal, and so was vision. The 
pupils reacted to light. She complained of difficulty with the 
lips, but could articulate fairly. She could not narrow the 
mouth to whistle as she formerly could. The voice was 
nasal. The arms were weak, the grasp with the dyna- 
mometer being only 10 kg. each. Extension of the fingers 
was the only movement distinctly deficient. They could not 
be straightened if the wrist was over-extended. Her legs 
were readily tired, but she could walk a mile. Her knee-jerks 
were afterwards found to be normal. There was little change 
in four years during which she was occasionally seen. Then 
she died, from what cause is unknown. 

Case ii. — A girl, aged twenty-nine, was sent to me on 
account of -general muscular feebleness, which was first 
noticed three years before, at twenty-six. The feebleness 
had come on gradually, in arms and legs, without change in 
sensation or affection of the sphincters. Her aspect at once 
attracted notice. There was double ptosis, so that the Kds 
concealed a third of the cornea, but the lids were sometimes 
fully raised. The eyes could not be moved upwards, and 



224 MYASTHENIA AND OPHTHALMOPLEGIA. 

very little downwards, the right eye could only be moved 
outwards to half the normal distance, the left eye still less. 
Convergence was lessened, and there was slight nystagmus 
on looking to the left. The pupils acted to light, and slightly 
on convergence, but accommodation was normal. The 
eyelids could be closed, but only feebly. The smile con- 
sisted only in elevation of the upper lip, the zygomatic 
muscles being apparently inactive, but a slight furrow oc- 
curred on the left side, perhaps from the risorius. The hps 
were weak, and she had lost her old ability of whistling. 
The voice was somewhat nasal, and the palate was but little 
raised on phonation. When the patient was tired, swallow- 
ing was difficult, and liquids occasionally regurgitated 
through the nose. The muscles of mastication were so 
readily fatigued that the patient had often to rest two or 
three times during a meal. The muscles of the neck were 
weak, and the head was kept upright with difficulty, tending 
to fall backwards or forwards. The arms were feeble, and 
if used quickly, became still more so. The legs were also 
weak, and she could only walk two or three hundred yards. 
A movement requiring force, such as flexion of the hip, could 
not be sustained for more than a few seconds. The knee- 
jerks were normal, and there w^as no foot clonus. There 
was no wasting. The electrical irritability of the muscles 
was normal and so was sensation. 

Besides nourishing food, she was treated with gentle 
massage, tonics, and the hypodermic injection of strych- 
nine. The result has been a slight but distinct improve- 
ment during the three years up to the present time. I have 
seen her at intervals of about six months, and without giving 
the details of her variations, I may describe her present state 
as observed in March, 1902. 

The patient's general condition was the same, but the 
improvement in many symptoms was conspicuous. The 



CASES. 225 

smile, levator only, was little changed except that on the 
left side, in laughing, there was the same shght outward 
movement of the angle of the mouth. The naso-labial 
furrow, on smiling, still extended from the nose to just above 
the corner of the mouth (see Fig. 16). The lips were dis- 
tinctly stronger; although she could not whistle even a year 
ago, she had done so on several occasions, loudly enough to 
call a dog. The tongue was protruded well, and the palate 
was raised a little better than nine months before. Fluids 
had ceased to regurgitate through the nose, the voice had 
lost its nasal character, and choking on swallowing had 
quite ceased. The masseters contracted strongly, but were 
soon tired, and the patient had still to rest from eating sev- 
eral times in the course of a meal. The ptosis continued 
and the eyelids could not be raised higher by the will, although 
still when she was interested, they were raised excessively, 
enough to show the sclerotic above the cornea. This was 
not attended by any overaction of the frontales, but the pa- 
tient could contract these shghtly by an effort of the will. 
The orbicularis could close the eyehds, but still with httle 
force; the contraction could be easily overcome. The move- 
ments of the eyes were as follows: Upward movement was 
absent in each; the downward movement was only a little 
less than normal (eighteen months before it was very slight). 
The right eye moved outwards (external rectus) about three- 
quarters of the normal distance, and the associated move- 
ment of the left eye (internal rectus) was about half the 
normal. The two eyes were moved to the left only about 
one-sixth of the normal, the same degree in each. The 
lateral movement of each eye separately was the same as 
when tested together. The lateral movements were attended 
with a curious disposition of the eyes to move downwards, 
greater when tested separately than together. No nystagmus 
could now be observed, but on looking to the left, the left 



226 MYASTHENIA AND OPHTHALMOPLEGIA. 

upper eyelid presented up and down nystagmoid movements. 
(I first noted this two years before in the same degree.) 
Convergence was weak; for an object 6 in. away the move- 
ment was only half the normal; it did not increase when the 
object was brought nearer, and soon diminished, the right eye- 
ball first moving outwards. The pupils reacted well to light 
and on convergence. Accommodation was fair, but seemed 
to be sooner exhausted in the right eye than in the left; there 
was shght hypermetropia. No weakness in the neck could 
now be observed, conspicuous as it was at first. The fingers 
could be completely extended, but the grasp Avas weak, 
although only slight evidence of exhaustion could be ascer- 
tained, successive efforts with the dynamometer resulting 
in a pressure of 15, 16, 17, 21, 14, 12, 13, and 14 kg. She 
had become able to write a long letter without fatigue, which 
was impossible two years before. In the legs, flexion of the 
hip was difficult; when sitting, the patient could only keep 
the foot, a few inches from the ground for two or three sec- 
onds. The flexors of the knee had fair power, although less 
than the extensors. The knee-jerks were active, and six 
repetitions caused no diminution. It was not practicable to 
test thoroughly the "myasthenic reaction," but the applica- 
tion of a tetanizing current to the extensors of the fingers 
for about a minute caused little indication of diminished irri- 
tability. In the zygomatic muscles, no contraction could be 
obtained on the left side, but only a slight trace on the right, 
and this may possibly have been due to stimulation of the 
risorius. The patient presented nowhere any local muscular 
atrophy, either in the trunk or limbs. She was thin, her 
weight being 98 lb. and height 5 ft. 6 in. — about two-thirds 
of the average weight for her height. 

These two cases present a striking resemblance, being of 
the same sex, not far apart in age, and alike in general and 
local symptoms, and in the course of these. Muscular 



REMARKS. 227 

cxhaustibility was not noted in the first case, probably be- 
cause it was not looked for. 

Case hi. — The last case differs from the others in the later 
age of the patient, thirty-nine (the symptom dating from 
thirty-seven), and the fact that the defective power in the 
limbs was much less prominent. Nevertheless, the resem- 
blance in the slight bulbar symptoms, in the condition of 
the face, and the defective movement of the eyes was so 
close as to show that it was of the same nature. It is not, 
however, worth while to describe it in detail since the 
account would be chiefly a repetition of the symptoms of 
the last case. The special features will be mentioned in 
the discussion of the particular symptoms. 

Remarks. 

I do not propose to discuss the general features of the 
disease. The question of its nature will be presently con- 
sidered, and the relation to it of the symptoms to which I 
desire especially to direct attention. These are the pecu- 
liarity of the lower facial movements in emotional expres- 
sion, and the defect in the movement of the eyes. 

The nasal smile is, perhaps, the most convenient designa- 
tion for the pecuhar character of the smile presented by each 
of these patients, although it might also be called the "levator 
smile." Its feature is the absence of the normal movement 
at the corner of the mouth, which either carries the furrow 
from the nose around the corner of the mouth or produces 
a separate depression there. In these patients the furrow 
of the smile was entirely above the upper lip, ceasing out- 
wards above the angle of the mouth. It is less marked in 
Case II than in either of the others, although I am only able 
to give an illustration of this case (Fig. 16). Its abnormal 



228 



MYASTHENIA AND OPHTHALMOPLEGIA. 



character may not be so conspicuous at first as when it is 
observed more closely, and especially when it is compared 
with the normal smile in a person of the same general aspect. 
Fig. 17 is from a photograph, which has been kindly taken 
for me by Dr. Farquhar Buzzard, of the effect of gentle 
faradic stimulation of the levator labii superioris in a patient 




Fig- 16. — From a photograph by 
Dr. Batterbury, of Berkham 
sted, of the patient Case ii, 
showing the limitation of the 
smile to elevation of the upper 
Up and the absence of move 
ment outwards of the angle of 
the mouth. The photograph 
gives only an imperfect indica- 
tion of this characteristic symp- 
tom. 



Fig. 17. — From a photograph by Dr. 
Farquhar Buzzard, showing the 
similar furrow caused by isolated 
stimulation of the levator labii 
superioris. 



whose face was anaesthetic in consequence of the removal of 
the Gasserian ganglion by Krause's operation. The slight 
contraction of the orbicularis palpebrarum is due to the fact 
that some of the branches to this muscle cannot be avoided. 
It will be seen that the furrow produced corresponds in posi- 
tion to that of the patient's smile. In Cases i and iii the 



REMARKS. 229 

limitation of the contraction to the muscles raising the upper 
lip was even more marked. In the case figured, on an 
energetic laugh, there was a slight movement on the left 
side of the mouth, probably by the risorius, which only 
made more conspicuous the absence of the normal move- 
ment. 

The fact that this nasal smile was so conspicuous in each 
of the cases raises the question whether it may not be a 
common feature of the disease. It does not seem to have 
attracted attention, but it might easily escape notice. In 
several recorded cases, "weakness of the lower facial mus- 
cles" is mentioned, without being definitely specified.* 

The Ophthalmoplegia. — Loss of power in the eyeball mus- 
cles has been mentioned as among the symptoms of many 
cases of myasthenia, but unfortunately has seldom been care- 
fully described. In these three cases it was a most con- 
spicuous and enduring symptom. It presents, at first sight, 
a strong resemblance to the ophthalmoplegia from nuclear 
degeneration. Yet there are some notew^orthy differences, 
possibly of much significance. One of these is the greater 
escape of the muscles moving the eyes downwards, and the 
implication in various degree of those moving the eyeballs 
upwards. Not less striking is the constant and irregular 
affection of the lateral muscles, the fact that this was different 
in degree in associated muscles, and that in some muscles it 



* This nasal smile or nasal snarl, as it might be called in its extreme form, 
bears a curious resemblance to the movement of the face by which most mon- 
keys express pleasure. This is well seen in the figures in Darwin's "Expres- 
sion of the Emotions." It raised the question whether animals possess zygo- 
matic muscles. By the kindness of Mr. Beddard, of the Zoological Gardens, 
Dr. Finny has made some dissections for me, which show that the zygomatic 
muscles are present in the animals, although they have not quite the same 
form as in man. How far their inaction in expression is the result of a dif- 
ference in their direction, consequent on the different shape of the face, is a 
question still to be decided. 



i^o MYASTHENIA AND OPHTHALMOPLEGIA. 

presented extraordinary variations at different periods. In 
order to present better these features, I have brought together 
the conditions in the three cases in a diagrammatic form 
which will be readily understood. Each outer circle repre- 
sents the normal extent of movement of the eye, and the 
length of the lines indicates the proportion which the actual 
movement bore to the normal. Where two or three lines are 
together they represent the variations of power at different 
times. 

In all cases the light-reflex of the iris was perfect, and I be- 
lieve that this has been the case in all recorded cases. The 
condition of accommodation was not easy to ascertain, on 
account of the presence of hypermetropia, but in two it 
seemed impaired, and the action of the pupil on accommo- 
dation seemed impaired with it, but the hindrance to con- 
vergence made the observations on this point uncertain. 

Ptosis was a marked feature, as in most cases, but there 
was no correspondence between its degree and the impair- 
ment of the upward movement of the eyes. Equally common 
was the weakness of the orbicularis palpebrarum, which was 
so marked in the second and third cases, while in the second 
case the weakness of the frontales was also conspicuous. 

My chief object is to call attention to the peculiar effect of 
the facial weakness, in altering the smile, and to the peculiar 
characters of the ophthalmoplegia, in the hope that future 
observers may ascertain how far these are common. I do 
not propose to discuss the pathology of the disease generally, 
but I may point out the possible bearing of the facts on the 
nature of the malady, a subject which remains altogether 
mysterious. 

The pathological problem is whether the symptoms de- 
pend upon a change in the muscles or in the nervous system, 



REMARKS. 



231 



or in both. The ''nasal smile" is only one feature of the 
distribution of the weakness of the facial muscles. The 




Fig. 18. — Diagrams to indicate the amount of movement of the eyes, Rand 
L, by the recti, in Cases i, 11, and in. The outer circle represents 
roughly the normal extent of movement in each direction. The Hues of 
diflFerent length placed together indicate the variations in the degree of 
the same movement at different periods of the case. 



significant fact regarding this is that it corresponds more 
closely to that met with in idiopathic muscular atrophy (mus- 



232 MYASTHENIA AND OPHTHALMOPLEGIA. 

cular dystrophy) than to known affections of the nervous 
system. This correspondence (which has been insisted on 
by Toby Cohn) is seen in the weakness of the frontales, the 
orbiculares palpebrarum and of the zygomatic muscles. 
The resemblance is strikingly shown by a comparison of the 
facial symptoms of myasthenia with the condition of the face 
in primary myopathy.* The latter, however long its dura- 
tion, does not involve of necessity any secondary changes in 
the motor nerves. Slight changes might, indeed, have 
been expected from the absence of function, but they are 
apparently not such as to be recognizable by any method 
of investigation. It is important to call attention to this 
fact, and the absolute weight of evidence of it presented 
by Spiller's case (among others), because it is very rare 
for a case to be so carefully observed during so long a period, 
and to become the subject of such careful pathological re- 
search. The facts also show how much caution is needed 
before assuming a simultaneous failure of vitality on the 
part both of the muscles and the motor nerves. 

A degeneration of the nerves involves also that of the 
muscles, and the coincidence of the two should only suggest 
that both are primary, when there is conclusive proof of 
truly simultaneous affection, which is not easily obtained. 

In myasthenia, the distribution of the symptoms in the 
muscles supplied from the medulla oblongata also corre- 



* Compare the facts mentioned in the lecture on Myopathy (p. 121). 
A very similar paralysis was present in the case figured in my "Manual," 3d 
edition, vol. i, p. 589, which is certainly a case of muscular dystrophy of 
the facial type (the type called that of Landouzy-Dejerine). It is equally 
striking in the remarkable case of this type which was described by Duch- 
enne in 1872, and also by Landouzy and Dejerine in 1886, and of which 
the pathological condition has only recently been described by SpiUer. 
The frontales and orbiculares were entirely degenerated, and the zygomatic 
muscles almost entirely. Complete as was the degeneration of a large 
number of the muscles, the motor nerves were absolutely normal. 



REMARKS. 233 

sponds to that in muscular dystrophy rather than in known 
central affections. A striking feature is the escape of the 
tongue and larynx, and the moderate degree of weakness of 
the hps and palate. In the cases I have here described, 
the variation in the degree of this weakness at difl'erent 
periods was as marked as was that of the eyeball muscles. 
The absence of perfect bilateral symmetry was as marked in 
the masseters, in one case, as in the eyeball muscles. 

But the ophthalmoplegia, from its resemblance to the 
nuclear form, may be regarded as suggestive of central dis- 
ease. It is important, therefore, to note the special features 
to which I have called attention. Future careful observa- 
tions may increase or diminish their significance. In its 
irregular distribution and variations, it presents some corre- 
spondence to the weakness in the muscles suppUed from the 
meduUa. It is, moreover, important to remember that the 
ocular muscles are part of the general muscular system. 
We are prone to associate them Avith the globes; they move 
in a special relation, but we know no reason why they 
should not suff'er in a widespread muscular malady. 

The information afforded by the microscope regarding the 
nature of the disease is purely negative. The latest methods 
of research disclose no structural change. This can surprise 
no one who has considered carefully the features of the 
malady. Where there is the capacity for normal action, 
although in diminished degree, normal structure would be 
anticipated, and an undue quickness of exliaustion would not 
be expected to be accompanied by visible alterations. The 
abihty for sustained exertion depends on the capacity for 
immediate renewal of the elements lost in function, a quick 
renewal by vital metabohsm. The exhaustibility in myas- 
thenia must depend upon defective capacity for this prompt 
vital nutrition, on a too tardy renewal of the molecules to 
permit exertion to be sustained. When we remember how 



^34 MYASTHENIA AND OPHTHALMOPLEGIA. 

far below discernment, or any promise of future discernment, 
the molecules of living tissue are, it will be realized how vast 
may be the imperfection of their nutrition, which can only 
be revealed by its functional effects. Hence we are only 
likely to obtain any pathological facts regarding the seat of 
the disease when local changes proceed far beyond the char- 
acteristic functional impairment and involve atrophic degen- 
eration. Atrophy of a few muscles has been noted in rare 
cases, irregular in distribution, but as yet they have afforded 
no reasons for regarding the malady as other than muscular. 

If present facts only enable us to regard myasthenia as a 
nutritional disorder, impairing the vital processes in the 
muscle, we should remember that this is hardly more than a 
statement of the obvious symptoms in pathological terms. 
It is only more by its implied negation of other morbid pro- 
cesses. The cause of this nutritional incapacity is, so far as 
we can yet see, the great problem of the disease, and it is 
the same, whether the malady is regarded as muscular or 
neural. Moreover, we must remember that nutritional dis- 
ease differs from organic degenerative disease only in de- 
gree. It consists in changes too fine to be discerned. It 
may differ in its capacity for recovery, but not in all cases, 
and not, usually, in myasthenia. 

The theory has been put forward and advocated that the 
impairment of function and vital nutrition can be best ex- 
plained by ascribing it to a toxic agent. The theory is in- 
definite, but is apparently based on the mysterious selective 
action of toxins, on the symmetry of their influence, and on 
the theory that the effects of fatigue are due to the production 
in the muscles of a toxic material. But when full weight is 
given to all these facts, their amount is very small. The argu- 
ment is purely one of analogy, a proverbial pitfall in reason- 
ing. All that it amounts to is that toxic influences may cause 
symptoms resembhng those of myasthenia in some super- 



REMARKS. ^35 

ficial characters. No one has yet suggested that muscular 
dystrophy has this origin, akhough it resembles myasthenia 
in some important features, among them in the symmetry 
on which so much weight is laid. The symmetry of the 
action of toxic agents depends on nutritional susceptibihty, 
and proves no more than this. It is very difficult for any 
one who has watched cases of myasthenia during years to 
conceive that the condition is due to a toxic agent, in the 
absence of any conceivable source for such an influence. 
The persistence of the symptoms, their slight inexplicable 
variations in detail and degree, make it difficult, at present, 
to go beyond the obvious fact of an imperfection in the vital 
nutritional power, which seems to be a defect of life, with 
little tendency to progress or improvement. We know, 
indeed, that many morbid states which have like manifes- 
tations may be brought about by divers causes, but where 
facts are few the need is all the greater for careful scrutiny 
of the evidence on which theories are ostensibly based. 

In recorded cases little benefit has seemed to result from 
any method of treatment. But in Cases ii and iii here 
described the effect of the hypodermic injection of strych- 
nine seemed distinct. Especially in Case ii its influence has 
been marked and sustained, and, in the opinion of the pa- 
tient, her friends, and her immediate medical adviser, admits 
of no doubt. In another case, quite similar in general 
features, its use has been attended by even greater im- 
provement, which seems enduring. 



LECTURE X. 

THE USE OF DRUGS. 

Delivered before the Harlesdon Medical Society on October ii, i8%. 



Mr. President and Gentlemen: — I am glad to have an op- 
portunity of addressing members of a branch of the pro- 
fession to which I have not the honour to belong, a Society 
of General Practitioners. The chief line of cleavage which 
runs through the profession is that which separates the 
many, whose work is primarily to apply knowledge, and 
the few, whose work it is primarily to advance knowledge, 
and also to apply, when needed, such particular knowledge 
as their work has enabled them to obtain. I use the word 
''honour" advisedly, because I hold that of the two branches, 
the general practitioner and the physician, the work of the 
general practitioner is the more deserving of honour. His 
work is, perhaps not more arduous, and perhaps, on the 
whole, has a more adequate practical reward, but it is 
destitute of the incentive which science supplies to those 
who serve her with pure heart and earnest endeavour, and 
which makes the labour, at least for such, its own reward. 
I have also used advisedly the word "particular" in con- 
trast to the word "general." The accurate antithesis would 
be "special." But this word now involves other concep- 
tions. I think, indeed, that those who are strong in their 
objection to specialism in medicine scarcely reahse how 
inevitable specialism is. It begins as soon as the boundary 

236 



THE GENERAL AND SPECIAL. 237 

of general practice is passed. The separation of medicine 
from surgery is itself specialism. But on this subject I 
need not dwell. I need not emphasise the necessity of 
restriction of range of work in order to secure depth, or 
the mistake that is made when speciahsm is confounded 
with exclusiyism. Yet I must, in passing, ask you neyer 
to forget the important fact that the special imphes the 
general, and that no man can be a true ''speciahst" who has 
not an adequate practical aquaintance with the whole range 
of at least one of the two great branches of professional 
knowledge. Eyery pro\ince of disease abounds in illus- 
trations of the degree to which the special inyolyes the 
general. In the case of sudden lesions of the brain, haemor- 
rhage or softening, the treatment needed is only in a small 
degree treatment of the neryous system. For the most 
part, it is treatment of the yascular system, or of the heart, 
or of the general blood state; and any good that can be 
done is to be effected only through a knowledge of all these 
morbid states and of their treatment. As a matter of fact, 
diseases of the neryous system, so called, are widening out 
into other proyinces in eyer-increasing degree. The extent 
to which symptoms directly of nervous nature depend upon 
blood states and constitutional conditions is becoming more 
and more apparent, and compels, not only wider knowledge, 
but greater familiarity with such diathetic states and their 
indications, many of which are only disclosed by their effect 
upon the neryous system. There is no part of medicine in 
which a so-called "nerye speciahst" must not be at home. 
No part of pathology is, or can be, isolated. Unless special 
work is based upon general and thorough knowledge, it is 
insecure, and those who trust to it are unsafe These facts 
should be recognised by practitioners. Consultants are, for 
the most part, that which practitioners, by their action, 
decide. 



238 THE USE OF DRUGS. 

It may occur to you that, in speaking of the general 
practitioner, I am speaking of that of which I know httle. 
But I count myself fortunate in having entered the pro- 
fession by the path which so few now tread — that of ap- 
prenticeship to a country practitioner. The changing times, 
the increased demands of the curriculum, and the long period 
of formal work, have made this method rare. Perhaps the 
change is wise. The first two years are now spent dif- 
ferently. And yet I learnt much which I would not have 
willingly foregone during the period in which my pro- 
fessional work consisted chiefly in dispensing medicines or 
assisting at a small operation. Summer afternoon rambles 
enabled me to do that which I have since found most useful 
— to learn much of practical British botany. Botany stands 
low among the subjects of medical study in professional 
estimation. But I am certain that there is no part of science 
which is indirectly of so much service as practical botany. 
The process of the identification of plants by the descrip- 
tions, the training it involves in accurate observation, in 
careful comparison, and in giving the proper relative weight 
to different features, is essentially the same as that which 
is needed in the diagnosis of disease. No subject affords 
mental training quite so effective for the practitioner's work. 

I also gained two perceptions of the work of the practi- 
tioner which I have never lost. The first is the narrow 
limit which circumstance sets to the therapeutical scope 
of the average practitioner. By "average practitioner" I 
mean the practitioner whose work is that of the majority, the 
work which lies among the lower classes, or among the lower 
middle classes. If the work of practitioners of this coun- 
try were measured by statistics, I believe these classes would 
make up four-fifths of it. Of such work, is not the following 
statement true? With the exception of the cases of acute 
disease, in which the means are more varied by which the 



THERAPEUTIC INFLUENCE. 239 

sufferer may be kept in life and be conducted back to health, 
the therapeutical means the practitioner can employ are 
almost limited to the administration of drugs. His means 
are almost restricted to the method of treatment to which 
it is now customary to refer in terms not far removed from 
those of contempt. Where is the room in such practice for 
the many measures of which we hear so much in the present 
day — massage and the like — measures which are developed 
in such elaboration of detail, and described in even a greater 
elaboration of terms ? These systems of treatment, of more 
or less utihty, pass in waves of fashion across the surface 
of suffering humanity with well-filled pockets. But they 
are not within the repertory of practitioners whose lot is cast 
in places less happy, and whose patients belong to classes 
less favoured. 

The second fact that was impressed upon me was that this 
method of treatment by drugs does, in a large number of 
cases, not only a definite but a great amount of good. This 
impression was derived from observation of the effects of 
such treatment in cases where observation is free from the 
complication of other influences, a source of fallacy inevit- 
able when patients are admitted to a hospital. When the 
administration of medicine was the only new element intro- 
duced into the problem, the good observed to follow may 
securely be assigned to it. This condition is often obtained 
in the treatment of hospital out-patients, and sometimes in 
the case of private patients. I beheve that those practi- 
tioners who closely watch the effects which follow, or seem to 
follow, the measures they adopt, will agree with me that the 
method of treatment to which the average practitioner is 
chiefly restricted has not only a power that can be realised 
now, but also a potentiahty yet to be developed. 

It has, therefore, been with great interest that I have 
seemed to see of late more clearly why this should be. The 



240 THE USE OF DRUGS. 

scepticism regarding the use of drugs to which I have referred, 
is, I think, less now than a few years ago. One favourite 
foothold was the statistical demonstration of inutihty, as, 
for instance, that the average duration of acute rheumatism 
was the same whatever treatment was employed or when 
no agents were used. Numbers must be great indeed to 
eliminate fallacy, and even statistics have failed to demon- 
strate the inutility of drugs, since help has been sought from 
the willow which casts its shadow on the damp places in 
which some forms of the malady lurk. We cannot doubt 
that that which has become true of one disease, definite con- 
trol by a fresh agent, will be true of others. The empirical 
advice, "Try all things; hold fast to that which is good," 
to which, in the hands of peasants, we owe many of our 
most precious aids, has been apphed to the results of modern 
chemistry, and many new products of science have been 
seized by the ''advanced pharmacy" of the present day, 
have been tried and found useful, although not often in the 
diseases in which they were expected to do good. 

But can we discern the reason why drugs are useful? 
Can we not, at least, discern the nature of the reason ? Here 
is a fact, the meaning of which is of far-reaching significance. 
I show you two tubes. Each contains a small quantity of 
a white powder — about half a teaspoonful. Each powder 
consists of the same elements, oxygen, hydrogen, nitrogen, 
and carbon. One is practically harmless; the other con- 
tains within it the power of death to looo men. The one 
is quinine; the other aconitia — the alkaloid which makes 
so deadly the plant whose flower our ancestors called "monks- 
hood," in the far-off days when the original was often before 
their eyes. It is an almost starthng fact that in this minute 
quantity of powder, hardly visible to those at a distance, 
there is such a potentiaHty of death. Picture to yourselves 
looo men. That which is in this tube would end the life of 



CHEMICAL POTENTIALITY. 241 

every one of them. Here is a latent power beside which the 
lightning flash is feeble, and to which the earthquake might 
give place, so far as the comparison depends on lethal cer- 
tainty. 

But the resemblance in the aspect of these two substances 
is not all. As I said, each consists of the same elements — 
each is made up of carbon, nitrogen, oxygen, and hydrogen. 
Each consists of the elements which compose air and water, 
with carbon added. \\Tiy is one almost harmless, and the 
other a most deadly poison? I might ask the question re- 
garding many other substances composed of the same ele- 
ments, but between these two the resemblance is strikingly 
close. The answer to my question may be given, ''It de- 
pends upon the chemical constitution." True, but this 
takes us a Ytry little way. When we discern that the differ- 
ence depends upon the way in which the elements are ar- 
ranged in molecules and the molecules are grouped together, 
we are not much nearer an explanation. We see a little 
more, however, when we reahse that chemical constitution 
means that energy is held ''latent" (as it is said), ready to 
be released when the elements form simpler, closer, com- 
pounds. All \^tal function of the body depends on a Hke 
simpler closer union of the elements which make up complex 
organic compounds. As far as we can see, all the energ}' 
which is released in the animal body is released in conse- 
quence of chemical action under the mysterious influence of 
life. Where such closer union of the elements and such re- 
lease of latent energ}' are going on, the process may be 
changed entirely by the contact of molecules of alhed con- 
stitution, with latent energy on the point of release, so held 
as to blend with that which is being set free in the living 
tissue. Blending T^-ith this, it may augment or oppose it. 
Remember that difference in chemical constitution means 
dift'erence in the readiness with which the elements separate 



242 THE USE OF DRUGS. . 

and reunite, and release their energy. Remember also that 
minute differences in constitution enable these chemical 
compounds then to blend with the vital action in one struc- 
ture, or to be absolutely inert. It must depend on differences 
in the vital chemistry which underlies function, although 
these differences which determine affinity or indifference we 
can discern only by the result.* 

Nerve force, as far as we can see, is the result of chemical 
changes occurring under the influence of life in the molecules 
which compose nerve tissue. Chemical processes, the break- 
ing up of complex compounds and the formation of simpler 
compounds, with consequent release of the energy held latent 
in the former, is the constant element in the production and 
conduction of nerve impulses. Some chemical compounds 
may come into relation with the tissue in which the 
change is occurring without exerting the slightest influence 
upon it. But another substance may come, even in amount 
inconceivably minute, whose molecules are so arranged as 
to fit in, as it were, with the changing molecules of the living 
tissue. The energy the new molecules bear seems to blend 
with that which is in process of ordered release in the living 
tissue, and to blend so effectively as to derange it entirely. 
The various nerve tissues which compose the centres seem 
to us the same, but they must differ in their precise chemical 
nature, and in the precise chemical action which their life- 
work involves. This fact is revealed to us only by their re- 
sponse to different chemical agents, and the result must be 
due to a difference in that on which the agent acts. Although 
we have no other evidence of this, consider the absolute 
significance of such facts as that atropine acts first upon the 
nerve substance of the eye, and strychnia upon that of the 



* The subject is considered in detail in " Dynamics of Life." London, 
Churchill's, 1894. 



MOLECULAR CONSTITUTION. 243 

spinal cord. Such an influence as I have spoken of seems 
to be exerted widely in the case of aconitia. Its contact with 
some acting nerve structures seems to be so instant and pre- 
cise as to induce the production of an excess of energy, 
sweeping all before it; on others, to oppose the process, to 
induce a sudden stillness among the changing molecules, and 
to arrest all action. Among the nerves thus influenced may 
be those on which depends the action of the heart, and with 
a sudden spasm or a sudden stillness, the heart stops and hfe 
is ended. That which so acts we call a poison. Widely 
different from this is that vehicle for energy which we call a 
food, yet the difference is one of degree. Every form of food 
is such by taking to the tissues new energy in fresh molecules. 
Between the two — the poison and the food — there is an almost 
infinite gradation of substances whose influence is exerted 
in the same way, by chemical compounds upon the chemical 
processes of life as well as on the state of nutrition, and on 
the mode of action of the living tissues. Between the two 
there is a like gradation, according to amount. It is in this 
intermediate region that there is the range of therapeutic 
influence conveyed by the vehicles we caU drugs. We think 
of these as forms of matter; we forget that matter is, to a large 
extent, merely a means of conveying energy. That which 
we term chemical constitution is the way in which energy is 
held, ready for release. It is by the relation of the latent 
energy of the agent to the energy being released in the tissue, 
and to the effect thus produced upon function, that one wide 
scope for the influence of drugs can be readily perceived. I 
think the facts we can discern justify the statement that 
treatment by drugs would be correctly named "dynamical 
therapeutics." 

Although what we call ''matter" is chiefly effective be- 
cause it is a vehicle for energy, we must remember that cer- 
tain elements are essential for its conveyance, and essential also 



244 THE USE OF DRUGS. 

for the maintenance of the nutrition of the tissues. In the 
functional action of all structures in the body, molecules are 
constantly passing off, which, having formed with oxygen 
lower compounds and having yielded their latent energy, are 
useless, and these are constantly being replaced by others, 
formed under the influence of life from the material which 
the plasma has brought to the vicinity of the tissue-elements. 
The constituents of some "poisons" may enter into the 
molecules of the tissues and thus disturb function by de- 
ranging the release of energy, and also derange structure. 
When arsenic is brought into contact with the nerve elements, 
whatever be its combination, it induces, first functional, and 
then structural changes in these, leading ultimately to their 
degeneration. We can only explain this by supposing that 
atoms of arsenic are taken up by the nerve substance in the 
course of the molecular renewal which attends functional 
action, "metabolism," it is called, and it is reasonable to 
suppose that this is due to its close relation to phosphorus, 
which we know is a constituent of the nerve material. It is 
possible that such substitution may take place in a slight 
degree without any injurious consequences, and even, in 
morbid states, with benefit. The influence on the nutri- 
tional process may be actually beneficial when this is already 
in some way deranged. It may perhaps promote the sub- 
sequent due assimilation of phosphorus, and make this more 
adequate and effective. Of course this is only a speculation. 
It is often useful to speculate when it is impossible to see. 

These remarks have reference of course only to the medi- 
cinal agents which act through the blood. There is a con- 
siderable scope for thought regarding the action of agents 
which do not pass into the blood, which act only upon the 
surface, or on that portion of our real exterior which is 
within us, as the alimentary canal. In this region, more- 
over, there is some room for bringing conception to the test of 



EMPIRICAL AND RATIONAL. 245 

experiment. Many purgatives, of course, act through the 
blood, but chemical processes seem to take less part in the 
operation of saline aperients. These act rather by "flush- 
ing out," the hquid in which the salt is dissolved being 
merely added to by osmosis. The subject, indeed, requires 
more special study than it has received. The great service 
of salines seems to me to be effected by removing that which 
would be in part reabsorbed. They carry away bile, much 
of which would pass back into the blood. This is doubtless 
true also of the purgatives. Some years ago it was said that 
the old idea that mercury reheves the liver was a mistake, 
because experiment showed that it did not increase the secre- 
tion of the bile. Yet the old idea was based upon a fact — 
that it does increase the amount of bile which leaves the body. 
This would pass back to the liver by the portal vein; by its 
removal the liver will be as effectually relieved as if its secre- 
tion were increased, perhaps indeed the rehef will be even 
greater. 

One other phase of modern therapeutical thought is the 
contrast which is often drawn between the empirical and the 
rational in the use of drugs, and the disparagement of the 
former in comparison with the latter. It is a comparison 
which deserves consideration. In part it is a result of the 
influence of the scientific training which now dominates 
medical education. Beneficial as this training is, its in- 
fluence may acquire a momentum that carries the effect too 
far for the good of those whose life is to be devoted to the 
hard and often routine work of applying knowledge. It is 
all very well to esteem the rational, but this esteem should 
not be allowed to cause an aversion from that which is 
precious, and yet cannot be called ''rational" in the com- 
mon, narrow sense of the word. The antithesis of the em- 
pirical and the rational is itself an error. It is an instance 



246 THE USE OF DRUGS. 

of a common tendency to put a negative conception into a 
positive word. Because the empirical is not the rational it 
is conceived as irrational — the only simple negative we have, 
but one that implies far more than mere absence of that 
which is excluded. The ''irrational" should be merely the 
"not rational"; it should mean only that for which an ex- 
planation cannot be discerned. In effect, it carries us as far 
beyond neutrality as does ''unreasonable." No one means 
by "unreasonable" a simple absence of the quality of reason- 
ableness; he means that which is opposed to reasonable. 
Not only is the empirical not positively irrational; it is doubt- 
ful how we are justified in considering that a truly rational 
element is absent from the empirical. The term "rational 
therapeutics" is applied to treatment in which a drug is given 
with success in accordance with preconceived ideas or theory. 
The theory may turn out quite wrong, although the result is 
the same. What, then, becomes of the rationality? In 
empirical therapeutics a drug is given because it is found by 
experience that in the particular condition it does good. 
Often we cannot even guess why. But the fact remains, and 
surely to act upon observed experience is as truly a rational 
proceeding as is action upon a theory which may be correct 
or incorrect. After all, the medicinal treatment which can 
be based upon any definite theory is small. How few are 
the drugs we can use to advantage which were not discovered 
by pure experience. In not one drug in twenty of those of 
most certain service can the use be traced to anything except 
unguided experiment. Our knowledge of these drugs, 
derived from the past, — and often from the distant past, — 
must be assumed to be the result of experiments innumerable, 
perhaps continued through the long centuries in which the 
human race has lived under the need to counteract disease 
by every available means. The need for food must itself 
have led to a knowledge of the physiological action of most 



PAST AND PRESENT. 247 

herbs of the field, and the habits of animals under obser- 
vation may often have had the force of example. It is 
probable that since man became able to observe and to 
reason, every common herb of the field and fruit of the tree 
has been at some time tested, and thus by slow degrees the 
knowledge of a physical good and evil has been acquired. 
It is strange, indeed, to note how far back goes the use of 
the drugs on which we most rely. Most of them can be 
traced far back into the distant past until they are lost in 
the blue mists which shroud alike the hills of Greece and the 
deserts of Arabia, or to the time when the world learnt its 
wisdom from the land where now the symbols of man's 
thought lie deep beneath the desert sand or stand silent 
in the cold moonhght of a long dead past. We smile at the 
popular herbal remedies. But it is to these that we owe the 
majority of our most useful drugs. I cannot conceive a 
therapeutist surveying a list of the chief drugs on which we 
depend in our daily work — and do not depend in vain — 
without a sense of wonder and perhaps of humiliation. We 
disinfect our rooms with burning sulphur; and so men did 
before the time of Homer. We purge sometimes with rhu- 
barb, especially when some subsequent astringent influence 
is desirable, and so did the old Arabians for the same special 
reason. The value of castor oil in its chief use was familiar, 
probably for ages, to the natives of the East and of the West 
Indies before it was made known in Europe by a physician 
from Antigua one hundred and fifty years ago. Aloes was 
employed in the same way long before the time of Dios- 
corides and Pliny. The knowledge of the influence of ergot 
in parturition we owe to the peasants of Germany, and the 
use of male-fern for tapeworm goes back to the old Greeks 
and Romans. The employment of mercury in syphilis by 
inunction and fumigation, which our nineteenth-century 
therapeutists regard with such satisfaction, seems to go back 



248 THE USE OF DRUGS. 

to the time of the Crusades, and it is said that its use can be 
traced in Malabar as far back as the ninth century. Podo- 
phyllum as a purgative we ov:e to the North American In- 
dians. If we go through all the drugs on which Ave most rely 
we find the same story. Even in the case of those which are 
the latest additions to our resources, we find that, with very 
few exceptions, their use arose from what we must regard as 
pure empiricism. It was by accident that the local anaes- 
thetic influence of cocaine was discovered. The unexpected 
results of simple experiment afforded us the chief use of 
antipyrin; and that which is perhaps the greatest practical 
discovery of modern times in the influence of drugs on dis- 
ease — the use of bromides in epilepsy — was the result of a 
chance observation of its use on an allied state — also em- 
pirical. Precisely the same statement is true regarding the 
employment of iodide in syphihs. It arose from an almost 
random trial of the influence of burnt sponge on goitre. 
To this day we are without any rational perception of their 
mode of action. I yield to no one in my sense of the im- 
portance of the rational in therapeutics; but we need to be 
careful lest, in contrasting the rational and the empirical, 
Ave alloAV our esteem for the one to induce a depreciation of 
the other. We can aft'ord to despise no source or kind of 
help, nor to permit our estimate to be prejudiced by the 
many warping influences to AA^hich our thought is liable. 

Any attempt to frame a definition of rational therapeutics 
will, I think, haAT one eft'ect. It can hardly fail to raise a 
doubt as to the propriety of considering that a theory to 
explain an empirical discoAxry makes the therapeutics 
rational. It is very easy to frame a theory of the action of 
a drug, and it is easy to extend this theory to the nature of 
the disease in which the drug does good, and at the same 
time to ignore the miany other possible AA'ays in AAdiich the 
eft'ect may be produced, and so to build from an uncertain 



EMPIRICAL AND RATIONAL. , 249 

foundation an edifice altogether unstable. When I recom- 
mend a drug I am often asked "How does it act?" Occa- 
sionally I can give some adequate reason, but I am gener- 
ally compelled to answer, "I do not know; it is often useful 
in this condition." Sometimes I can add, "There are several 
ways in which it may act." Sometimes I am obliged to say, 
"I have no idea how it does good." It has not been my 
privilege to add much to our therapeutical resources, but the 
few agents I have recommended have been based on pure 
empiricism. Many observers have confirmed the statement 
which I made more than twenty years ago regarding the 
occasional service of borax in epilepsy. In inveterate 
cases which do not yield to bromide, borax sometimes does 
good that is definite and distinctly greater than that which 
bromide produces in those patients. But I cannot say why. 
It was one of the many things I tried, simply as a peasant 
might try in succession a number of herbs. Further, the 
diminution in the tendency to the distressing pains in loco- 
motor ataxy which is caused by the regular administration 
of chloride of aluminium is so distinct that I have little 
doubt that the time will come when this drug will find a 
place in the Pharmacopoeia. But I had no other reason 
for trying it than the fact that some analogue suggested it. 
Of the rational we have here no trace, although I should 
take objection to the difference involved in the application 
of the epithet "irrational." 

There is much more I should like to say for which time 
fails. I must content myself with expressing the hope that 
you will endeavour to apply what I have suggested to you. 
I feel sure that such a Society cannot do more for its 
members, and cannot in any way do more for the pro- 
fession outside, than by carefully considering what drugs 
are found, by the personal experience of each one, to be of 
real use, by combining the results of personal observation 



250 . THE USE OF DRUGS. 

and by endeavouring in the future to organise mutual help 
in respect to the new therapeutic agents which are bestowed 
upon us by the earnestness and energy of others. 

I count it a high privilege to teach, but a privilege far 
higher to help men to teach themselves. It is easy to lose 
that which is merely received. That which is acquired is 
persistent. Knowledge personally gained becomes part of 
a man's mental self — not only as knowledge, but as power. 
It rises in its influence into every branch of the complex 
activity of practical life, and it becomes effective through its 
indirect effect even where we cannot trace its presence. 



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SUBJECT INDEX. 



Gould's Medical Dictionaries, - Pages 12, 13 
Morris' Anatomy, New Edition, - - Page 4 
Compends for Students, - - - - Page 27 



BUBJICT. PAOS 

Alimentary Canal (see S\ir- 

gery) 24 

Anatomy 7 

Anesthetics 18, 19 

Autopsies (see Pathology) 20 

Bacteriology 8 

Bandagring (see Surgery) . . 24 
Blood, Examination of. . . 8 

Brain 8 

Chemistry. Physics .... 9 

Children, Diseases of 11 

Climatology 19 

Clinical Charts 25 

Compends 27 

Consumption (see Lungs) . 16 
Cyclopedia of Medicine ... 13 

Dentistry 11 

Diabetes(seeUrin. Organs) 25 

Diagnosis 11 

Diagrams (see Anatomy) . 8 
Dictionaries, Cyclopedias. 12 

Diet and Food 13 

Disinfection 16 

Dissectors 7 

Ear 14 

Electricity 14 

Embryology 7 

Emergencies 24 

Eye 14 

Fevers 15 

Food 13 

Formxilaries 21 

Gynecology 15 

Hay Fever 25 

Heart 15 

Histology 15 

Hydrotherapy 19 

Hygiene 16 

Hypnotism 8 

Insanity 8 

Intestines 23 

Latin, Medical (see Phar- 
macy) 21 

Life Insurance 19 

Limgs 16 

Massage 17 

Materia Medica 17 

Mechanotherapy ........ 17 

Medical Jurisprudence .... 18 



SUBJECT. PAQB 

Mental Therapeutics 8 

Microscopy 18 

Milk 8, 10 

Miscellaneous 18 

Nervous Diseases 19 

Nose 25 

Nuraing 20 

Obstetrics 20 

Ophthalmology 14 

Organotherapy 18 

Osteology (see Anatomy). 7 

Pathology 20 

Pharmacy 21 

Physical Diagnosis 11 

Physical Training 17 

Physiology 22 

Pneumotherapy 19 

Poisons (see Toxicology) . . 18 

Practice of Medicine 22 

Prescription Books (Phar- 
macy) 21 

Refraction (see Eye) 14 

Rest 19 

Sanitary Science ra 16 

Serum-Therapy 17 

Skin 23 

Spectacles (see Eye) 14 

Spine (see Nervous Dis- 
eases) 19 

Stomach 23 

Students' Compends 27 

Sxirgery and Surgical Dis- 
eases 24 

Technological Books ..... 9 

Temperature Charts 25 

Therapeutics ........... 17 

Throat 25 

Toxicology 18 

Tumors (see Siu-gery) .... 24 

U. S. Pharmacopoeia 22 

Urinary Organs 25 

Urine 25 

Venereal Diseases 26 

Veterinary Medicine 26 

Visiting Lists, Physicians'. 
{Send for Special Circu- 
lar.) 

Water Analysis 16 

Women, Diseases of 15 



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SUBJECT CATALOGUE OF MEDICAL BOOKS. 7 

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MEDICAL BOOKS. 11 



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becility, Insanity, etc. 2d Edition. $4.00 
POWER. Surgical Diseases of Children and their Treatment 
by Modem Methods. Illustrated. $2.50 
STARR. The Digestive Organs in Childhood. The Diseases of 
the Digestive Organs in Infancy and Childhood. 3d Edition, 
Rewritten and Enlarged. Illustrated. $3.00 
STARR. Hygiene of the Nursery. Including the General Regi- 
men and Feeding of Infants and Children, and the Domestic 
Management of the Ordinary Emergencies of Early Life, 
Massage, etc. 6th Edition. 25 Illustrations. $1.00 
SMITH. Wasting Diseases of Children. 6th Edition. $2.00 
TAYLOR AND WELLS. The Diseases of Children. 2d Edition, 
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**It is well worthy the careful study of both student and prac- 
titioner, and can not fail to prove of great value to both. We 
do not hesitate to recommend it." — Boston Medical and Surgical 
Journal. 

DIAGNOSIS. 

BROWN. Medical Diagnosis. A Manual of Clinical Methods. 
4th Edition. 112 Illustrations. Cloth, $2.25 

DA COSTA. Clinical Hematology. A Practical Guide to Exam- 
ination of Blood, with Reference to Diagnosis. 6 Colored 
Plates, 48 other Illustrations. Cloth, $5.00 ; Sheep, $6,00 

DOUGLAS. Surgical Diseases of Abdomen, with Reference to 
Diagnosis. 20 Full-Page Plates. Just Ready. 

Cloth, $7.00 ; Sheep, $8.00 

EMERY. Bacteriological Diagnosis. 2 Colored Plates and 32 
other Illustrations. $1.50 

MEMMINGER. Diagnosis by the Urine. 2d Ed. 24 lUus. $1.00 

PERSHING. Diagnosis of Nervous and Mental Diseases. 
Illustrated. $1.25 

STEELL. Physical Signs of Pulmonary Disease. $1.25 

TYSON. Handbook of Physical Diagnosis. For Students and 
Physicians. By the Professor of Clinical Medicine in the Uni- 
versity of Pennsylvania. Illus. 4th Ed., Improved and En- 
Uu'ged. With 2 Colored and 55 other Illustrations. $1.50 

DENTISTRY. 

Special Catalogue of Dental Books tent free upon application. 
BARRETT. Dental Surgery for General Practitioners and 
Students of Medicine and Dentistry. Extraction of Teeth, 
etc. 3d Edition. lUustrated. $1.00 



12 SUBJECT CATALOGUE. 

BROOMELL. Anatomy and Histology of the Human Mouth 
and Teeth. Second Edition, Revised and Enlarged. 337 
handsome Illustrations. Cloth, $4.50; Leather, $5.50 

FILLEBROWN. Operative Dentistry. Illustrated. $2.25 

GORGAS. Dental Medicine. A Manual of Materia Medica and 
Therapeutics. 7th Edition. Cloth, $4.00; Sheep,$5.00 

GORGAS. Questions and Answers for the Dental Student. 
Embracing all the subjects in the Curriculum of the Dental 
Student. Octavo. $6.00 

HARRIS. Principles and Practice of Dentistry. Including 
Anatomy, Physiology, Pathology, Therapeutics, Dental Sur- 
gery, and Mechanism. 13th Edition. Revised by F. J. S. 
GoHQAS, M.D., D.D.s. 1250 Illus. Cloth, $6.00 ; Leather, $7.00 

HARRIS. Dictionary of Dentistry. Including Definitions of Such 
Words and Phrases of the Collateral Sciences as Pertain to the 
Art and Practice of Dentistry. 6th Edition, Revised and 
Enlarged by Ferdinand J. S. Gorqas, m.d., d.d.s. 

Cloth, $5.00; Leather, $6.00 

RICHARDSON. Mechanical Dentistry. 7th Edition. Thor- 
oughly Revised and Enlarged by Dr. Gbo. W. Warrkn. 691 
Illustrations. Cloth, $5.00; Leather, $6.00 

SMITH. Dental Metallurgy. 2d Edition. Illustrated. $2.00 

TAFT. Index of Dental Periodical Literature. $2.00 

TOMES. Dental Anatomy. 263 Illustrations. 5th Ed. $4.00 

TOMES. Dental Surgery. 4th Edition. 289 Illus. $4.00 

WARREN. Compend of Dental Pathology and Dental Medicine. 
With a Chapter on Emergencies. 4th Edition. Illustrated. 

.80; Interleaved, $1.00 
WARREN. Dental Prosthesis and Metallurgy. 129 Illus. $1.25 
WHITE. The Mouth and Teeth. Illustrated. .40 

DICTIONARIES. CYCLOPEDIAS. 

GOULD. The Illustrated Dictionary of Medicine, Biology, and 
Allied Sciences. Being an Exhaustive Lexicon of Medicine and 
those Sciences Collateral to it: Biology (Zoology and Botany), 
Chemistry, Dentistry, Pharmacology, Microscopy, etc., with 
many useful Tables and numerous fine Illustrations. 1633 
pages. Fifth Edition. ^ 

Sheep or Half Morocco, $10.00; with Thumb Index, $11.00 
Half Russia, Thimib Index, $12.00 
GOULD. The Medical Student's Dictionary, nth Edition. Il- 
lustrated. Including those Words and Phrases generally used 
in Medicine, with their Proper Pronunciation and Definition, 
Based on Recent Medical Literature. With Table of Epo- 
njnoaic Terms and Tests and Tables of the Bacilli, Micrococci, 
Mineral Springs, etc., of the Arteries, Muscles, Nerves, Ganglia, 
Plexuses, etc. Eleventh Edition. Enlarged and illustrated 
with a large number of Engravings. 840 pages. 

Half Morocco, $2.60 ; with Thumb Index, $3.00 
Flexible"Leather, Burnished Edges, Thumb Index, 3.50 



MEDICAL BOOKS. 13 



GOULD. The Pocket Pronouncing Medical Lexicon. 4th Edi- 
tion. (30,000 Medical Words Pronounced and Defined.) Con- 
taining all the Words, their Definition and Pronunciation, 
that the Medical, Dental, or Pharmaceutical Student Gener- 
ally Comes in Contact with; also Elaborate Tables of Epo- 
nymio Terms, Arteries, Muscles, Nerves, BacUli, etc., etc., a 
Dose List in both English and Metric Systems, etc., Arranged 
in a Most Convenient Form for Reference and Memoriaing. 
Fourth Edition, Revised and Enlarged. 838 pages. 
Full Limp Leather, Gilt Edges, $1.00; Thumb Index, $1.25 
145,000 Copies of Gould's Dictionaries have been sold. 

GOULD AND PYLE. Cyclopedia of Practical Medicine and 
Surgery. Seventy-two Special Contributors. Illustrated. One 
Volume. A Concise Reference Handbook of Medicine, Sur- 
gery, Obstetrics, Materia Medica, Therapeutics, and the Vari- 
ous Specialties, with Particular Reference to Diagnosis and 
Treatment. CompUed under the Editorial Supervision of 
Gborob M. Gould, m.d., Author of "An Illustrated Dictionary 
of Medicine," etc.; and Waltbr L. Ptlb, m.d., Assistant 
Siirgeon Wills Eye Hospital; formerly Editor "International 
Medical Magazine," etc., and Seventy-two Special Contribu- 
tors. With many Illustrations. Large Square 8vo, to corre- 
spond with Gould's "Illustrated Dictionary." 
Full Sheep or Half Mor., $10.00; with Thumb Index, $11.00 
Half Russia, Thumb Index, $12.00 net. 

GOULD AND PYLE. Pocket Cyclopedia of Medicine and Sur- 
gery. Based upon above book and imiform in size with 
"Gould's Pocket Dictionary." 

Full Limp Leather, Gilt Edges, $1.00 
With Thumb Index, $1.25 

ECARRIS. Dictionary of Dentistry. Including Definitions of 
Such Words and Phrases of the Collateral Sciences as Pertain 
to the Art and Practice of Dentistry. 6th Edition, Revised 
and Enlarged by Fkhdinand J. S. Gorqas, m.d., d.d.s. 

Cloth, $5.00; Leather, $6.00 

LONGLEY. Pocket Medical Dictionary. Cloth, .75 

TREVES AND LANG. German-English Medical Dictionary. 

Half Calf, $3.25 

DIET AND FOOD. 

ALLEN. Proteids and Albuminous Principles. An analytical 
Study of Food Products. 2d Edition. $4.50 

BURNETT. Foods and Dietaries. A Manual of Clinical Diet- 
etics, with Diet Lists for Various Diseases, etc. 2d Ed. $1.50 

DAVIS. Dietotherapy. Food in Health and Disease. With 
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Physiologic Therapeutics, page 17. 

GREENISH. Microscopical Examination of Foods and Drugs. 

Illustrated. Jtist Ready. $3.50 

HAIG. Diet and Food. Considered in Relation to Strength and 
Power of Endurance. 4th Edition. $1.00 

LEFFMANN. Select Methods in Food Analysis. Ulus. $2.50 



14 SUBJECT CATALOGUE. 

EAR (see also Throat and Nose). 

BURNETT. Hearing and How to Keep It, Illustrated. .40 

HOVELL. Diseases of the Ear and NasorPharynx. Including 
Anatomy and Physiology of the Organ, together with tha 
Treatment of the Affections of the Nose and Pharynx which 
Conduce to Aural Disease. 128 Illustrations. 2d Ed. $5.50 
PRITCHARD. Diseases of the Ear. 4th Edition, Enlarged. 
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2d Edition. $1.00 

HEDLEY. Therapeutic Electricity and Practical Muscle Testing. 

99 Illustrations. $2.50 

JACOBY. Electrotherapy. 2 volumes. Illustrated. See Cohen, 

Physiologic Therapeutics, page 17. 
JONES. Medical Electricity. 3d Edition. 117 Illus. $3.00 

EYE. 

A Special Circular of Books on the Eye sent free upon application. 

DARIER. Ocular Therapeutics. Just Ready. $3.00 

DONDERS. The Nature and Consequences of Anomalies of 
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FICK. Diseases of the Eye and Ophthalmoscopy. Translated 
by A. B. Halb, m.d. 157 Illus. Cloth, $4.50; Sheep, $5.50 

GOULD AND PYLE. Compend of Diseases of the Eye and Re- 
fraction. Including Treatment and Operations, and a Section 
on Local Therapeutics. With Formulae, Useful Tables, a 
Glossary, and 111 lUus., several of which are in colors. 2d 
Edition, Revised. Cloth, .80; Interleaved, $1.00 

GREEFF. The Microscopic Examination of the Eye. lUua- 
trated. $1.25 

HARLAN. Eyesight, and How to Care for It. Illus. .40 

HARTRIDGE. On the Ophthalmoscope. 4th Edition. With 
4 Colored Plates and 68 Wood-cuts. $1.60 

HARTRIDGE. Refraction. 104 Illustrations and Test Types. 
12th Edition, Enlarged. $1.50 

HANSELL AND SWEET. Treatise on Diseases of the Eye. 
With 253 Illustrations. $4.00 

HANSELL AND REBER. Muscular AnomaUes of the Eye. 
lUustrated. $1.50 

HANSELL AND BELL. Clinical Ophthalmology. Colored 
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HENDERSON. Notes on the Eye. 3d Ed. Just Beady. $1.50 

JENNINGS. Manual of Ophthalmoscopy. 95 Illustrations and 
1 Colored Plate. $1.50 

MORTON. Refraction of the Eye. Its Diagnosis and the Cor- 
rection of its Errors. 6th Edition. $1.00 

OHLEMANN. Ocular Therapeutics. Authorized Translation, 
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PARSONS. Elementary Ophthalmic Optics. With Diagram- 
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MEDICAL BOOKS. 15 

PHILLIPS. Spectacles and Eyeglasses. Their Prescription 
and Adjustment. 3d Edition. 52 Illustrations. $1.00 

SWANZY. Diseases of the Eye and Their Treatment. 8th 
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Plate and a ZephjT Test Card. Just Ready. $2.50 

THORINGTON. Retinoscopy. 4th Edition, Carefully Revised. 
Illustrated. $1.00 

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tions, 13 of which are colored. 2d Edition. $1.50 

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WORTH. Squint : Its Causes, Pathology, Treatment. $2.00 

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117 Illustrations and a Glossary. $3.00 

FEVERS. 

GOODALL AND WASHBOURN. Fevers and Their Treatment. 

Illustrated. $3.00 

WILCOX. Fever Nursing. In Press. 

GYNECOLOGY. 

BISHOP. Uterine Fibromyomata. Their Pathology, Diag- 
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BYFORD (H. T.). Manual of Gynecology. 3d Edition, Revised 
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trationa. $1.50 

FULLERTON. Surgical Nursing. 3d Edition, Revised and 
Enlarged. 69 Illustrations. $1.00 

GALABIN. Diseases of Women. Sixth Edition. By Alfred 
Lewis Galabin, m.a., m.d., f.r.c.p. 6th Edition, Revised 
and Enlarged. 284 Illustrations. Octavo. Cloth, S5.00 

LEWERS. Diseases of Women. 146 Illus. 5th Ed. $2.50 

LEWERS. Cancer of the Uterus. Just Ready. $3.00 

MONTGOMERY. Practical Gynecology. A Complete Sys- 
tematic Text-Book. 2d Edition, Revised and Enlarged. 
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ROBERTS. Gynecological Pathology. With 127 Full-page 
Plates containing 151 Figures. $6.00 

WELLS. Compend of Gynecology. Illustrated. 3d Edition, 
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HEART. 

THORNE. The Schott Methods of the Treatment of Chronic 
Heart Disease. Fourth Edition. Illustrated. $2.00 

HISTOLOGY. 

CUSHING. Compend of Histology. By H. H. Cushins, m.©., 
Demonstrator of Histology, Jefferson Medical College, Phila- 
delphia. Illus. Nearly Ready. .80; Interleaved, $1.00 

LAZARUS-BARLOW. Pathological " Anatomy and Histology. 
Illustrated. . Jttst Ready. $6.50 



1« SUBJECT CATALOGUE. 

STIRLING. Outlines of Practical Histology. 368 Illustrations. 
2d Edition, Revised and Enlarged. With new Illua. $2.00 

STOHR. Histology and Microscopical Anatomy. Edited by 
A. ScHAPBR, M.D., University of Breslau, formerly Demon- 
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HYGIENE. 

Special Catalogue of Books on Hygiene sent free upon application. 

CANFIELD. Hygiene of the Sick-Room. A Book for Nurses 
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lation, etc. $1.25 

CONN. Agricultural Bacteriology. Illustrated. $2.50 

CONN. Bacteriology of Milk and Milk Products. Illus. $1.26 

COPLIN. Practical Hygiene. A Complete American Text- 
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LEFFMANN. Select Methods in Food Analysis. 63 Illustra- 
tions and 4 Plates. $2.50 

LEFFMANN. Examination of Water for Sanitary and Technical 
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LEFFMANN. Analysis of Milk and Milk Products. Illustrated. 
Second Edition. $1.25 

LINCOLN. School and Industrial Hygiene. .40 

McFARLAND. Prophylaxis and Personal Hygiene. Care of 
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NOTTER. The Theory and Practice of Hygiene. 15 Plates and 
138 other Illustrations. 8vo. 2d Edition. $7.00 

PARKES AND KENWOOD. Hygiene and PubUc Health. 2d 
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ROSENAU. Disinfection and Disinfectants. Illus. $2.00 

STARR. The Hygiene of the Nursery. Including the General 
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LUNGS AND PLEURA. 

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Treatment in Special Institutions and at Home. Illus. $3.00 

STEELL. Physical Signs of Pulmonary Disease. Illua. $1.26 



MEDICAL BOOKS. 17 



MASSAGE. PHYSICAL EXERCISE. 

OSTROM. Massago and the Orifi:inal Svredish Movements. 
Their Application to Varioiis Diseases of the Body. A Manual 
for Students, Nurses, and Physicians. Fifth Edition, En- 
larged. 115 Illustrations, many of which are original. Jl.OO 

MITCHELL AND GULICK. Mechanotherapy. Exercise, Ortho- 
pedics, Massage, Ocular Corrections, etc. Illustrated. See 
Cohen, Physiologic Therapeutics, below. 

TREVES. Physical Education. Its Value, Method*, etc. .75 

MATERIA MEDICA AND THERAPEUTICS. 

BRACKEN. Outlines of Materia Medica and Pharmacology. $2.75 
COBLENTZ. The Newer Remedies. Including their Synonyms, 
Sources, Methods of Preparation, Tests, Solubilities, Doses, 
etc. 3d Edition, Enlarged and Revised. $1.00 

COHEN. Physiologic Therapeutics. Methods other than Drug- 
Giving useful in the Prevention of Disease and in the Treat- 
ment of the Sick. Mechanotherapy, Mental Therapeutics, 
Suggestion, Electrotherapy, Climatology, Hydrotherapy, 
Pneumatotherapy, Prophylaxis, Dietetics, Organotherapy, 
Phototherapy, Mineral Waters, Baths, etc. 11 volumes, 8vo. 
Illustrated. (Subacription.) Cloth, $27.60; i Mor., $38.50 

Special Descriptive Circular v>ill be sent upon application. 
GORGAS. Dental Medicine. A Manual of Materia Medica and 
Therapeutics. 7th Edition, Revised. " $4.00 

GROFF. Materia Medica for Nurses, with Questions for Self- 
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HELLER. Essentials of Materia Medica* Pharmacy* and Pre- 
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HEWLETT. Serum-Therapy. $1.75 
MAYS. Theine in the Treatment of Neuralgia, i boimd. .50 
POTTER. Handbook of Materia Medica. Pharmacy, and Thera- 
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Formulae. 9th Edition, Revised and Enlarged. With Thumb 
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discusses a good naany drugs which are rarely employed, and 
therefore the book is as useful to one who wishes to look for un- 
usual information as it is to him who wishes a handbook for ready 
reference in the treatment of disease as he meets it from day to 
day." — Therapeutic Gazette. 

POTTER. Compend of Materia Medica, Therapeutics, and Pre- 
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Action of Drugs. 6th Edition. .80; Interleaved, $1.00 

MURRAY. Rough Notes on Remedies. 4th Edition. $1.25 

SAYRE. Organic Materia Medica and Pharmacognosy. An 
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oal Botany. With sections on Histology and Microtechnique, 
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original. 2d Edition. Cloth, $4.50 



18 SUBJECT CATALOGUE. 

TAVERA. Medicinal Plants of the Philippines. $2.00 

WHITE AND WILCOX. Materia Medica, Pharmacy, Pharma- 
cology, and Therapeutics. 5th American Edition, Revised by 
Rbtnold W. Wilcox, m.a., m.d., ll.d.. Professor of Clinical 
Medicine and Therapeutics at the New York Post-Graduate 
Medical School. Cloth, $3.00 ; Leather, $3.50 

MEDICAL JURISPRUDENCE AND 
TOXICOLOGY. 

REESE. Medical Jurisprudence and Toxicology. A Text-Book 
for Medical and Legal Practitioners and Students. 6th 
Edition. Revised by Henrt LurFMANN. m.d. 

Cloth, $3.00; Leather, $3.50 
"To the student of medical jiu-isprudence and toxicology it in 

invaluable, as it is concise, clear, and thorough in every respect." 

— The American Journal of the Medical Sciences. 

MANN. Forensic Medicine and Toxicology. lUxis. $6.50 

TANNER. Memoranda of Poisons. Their Antidotes and Tests. 

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MICROSCOPY. 

CARPENTER. The Microscope and Its Revelations. 8th 
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Plates. Cloth, $8.00 ; Half Morocco, $9.00 

GREENISH. Microscopical Examination of Foods and Drugs. 
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LEE. The Microtomist's Vade Mecum. A Handbook of 
Methods of Microscopical Anatomy. 887 Articles. 5th 
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OERTEL. Medical Microscopy. A Guide to Diagnosis, Ele- 
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REEVES. Medical Microscopy, including Chapters on Bacteri- 
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WETHERED. Medical Microscopy. A Guide to the Use of the 
Microscope in Practical Medicine. 100 Illustrations. $2.00 

MISCELLANEOUS. 

BERRY. Diseases of Thyroid Gland. Illustrated. $4.00 

BUXTON. Anesthetics. Illustrated. 3d Edition. $1,50 

COHEN. Organotherapy. See Cohen, Physiologic Therapeutic*, 

page 17. 
FRENKEL. Tabetic Ataxia. Illustrated. $3.00 

GOULD. Borderland Studies. Miscellaneous Addresses and 
EfiSAys. 12mo. $2.00 

GOULD. Biographic Clinics. Volume I. The Origin of the 
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Browning. $1.00 



MEDICAL BOOKS. 18 

GOULD Biographic Clinics. Volume II. The Origin of the 
Ill-Health of Wagner, Parkman, Mrs. Carlisle, Spencer, 
Whittier, Ossoli, George Eliot, and Nietsche. Nearly Ready. 
GREENE. Medical Examination for Life Insurance. lUus. 
With colored and other Engravings. 2d Edition. In Press. 
HAIG. Causation of Disease by Uric Acid. The Pathology of 
High Arterial Tension, Headache, Epilepsy, Gout, Rheuma- 
tism, Diabetes, Bright's Disease, etc. 6th Edition. $3.50 
HENRY. A Practical Treatise on Anemia. Half Cloth, .50 

NEW SYDENHAM SOCIETY'S PUBLICATIONS. Circulars 
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OSGOOD. The Winter and Its Dangers. .40 

PACKARD. Sea Air and Sea Bathing. .40 

RICHARDSON. Long Life and How to Reach It. .40 

SCHEUBE. Diseases of Warm Countries. Illustrated. Just 
Ready. $8.00 

TISSIER. Pneumotherapy, Aerotherapy, Inhalation Methods. 

See Cohen, Phyaiologic Therapeutics, page 17. 
TURNBULL. Artificial Anesthesia. 4th Ed. Illus. $2.50 

WARDEN. The Paris Medical School. Paper, .75 

WEBER AND HINSDALE. Climatology and Health Resorts. 
Including Mineral Springs. 2 vols. Illustrated with Colored 
Maps. See Cohen, Physiologic Therapeutics, page 17. 
WILSON. The Summer and Its Diseases. .40 

WINTERNITZ. Hydrotherapy, Thermotherapy, Phototherapy, 
Mineral Waters, Baths, etc. Illustrated. See Cohen, Physio- 
logic Therapeutics, page 17. 

NERVOUS DISEASES. 

DERCUM. Rest, Suggestion, Mental Therapeutics. See Cohen, 
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GORDINIER. The Gross and Minute Anatomy of the Central 
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GOWERS. Epilepsy and Other Chronic Convulsive Diseases. 
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PRESTON. Hysteria and Certain AUied Conditions. Their 
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WOOD. Brain Work and Ortrwork. .40 



20 SUBJECT CATALOGUE. 

NURSING (see also Massage). 

Special Catalosrue of Book* for Nurse* tent fr«* upon applieation. 

CAIfFIELD. Hygiene of the Sick-Room. A Book for Nurses 
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Ventilation, and Eandred Subjects for the Use of Nurses and 
Other InteUigent Women. $1.25 

CUFF. Lectxires to Nurses on Medicine. 4th Edition. $1.25 

DAVIS. Bandaging. Its Principles and Practice. 163 Original 
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DOMVILLE. Manual for Nurses and Others Engaged in At- 
tending the Sick. 9th Edition. With Recipes for Sick-room 
Cookery, etc. In Pre**. 

FULLERTON. Obstetric Nursing. 6th Ed. 45 Illus. $1.00 

FULLERTON. Surgical Nursing. 3d Ed. 69 lUus. $1.00 

GROFF. Materia Medica for Nurses. With Questions for Self- 
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Ready. $1.25 

HADLEY. General, Medical, and Surgical Nursing. A very 
Complete Manual, Including Sick-room Cookery. $1.25 

HUMPHREY. A Manual for Nurses. Including General 
Anatomy and Physiology, Management of the Sick-room, etc. 
24th Edition. 79 Illustrations. $1.00 

STARR. The Hygiene of the Ntu-sery. Including the General 
Regimen and Feeding of Infants and Children, and the Domes- 
tic Management of the Ordinary Emergencies of Early Life, 
Massage, etc. 6th Edition. 25 Illustrations. $1.00 

TEMPERATURE AND CLINICAL CHARTS. See page 25. 

VOSWINKEL. Surgical Nursing. Second Edition, Enlarged. 
112 Illustrations. $1.00 

WILCOX. Fever Nursing. Preparing. 

OBSTETRICS. 

CAZEAUX AND TARNIER. Midwifery. With Appendix by 
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Diseases of Pregnancy and Parturition, Obstetrical Operations, 
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Plates, and numerous Wood Engravings. 

Cloth, $4.50; Full Leather, $5.50 

EDGAR. Text-Book of Obstetrics. By J. Cufton Edgar, 
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WINCKEL. Text-Book of Obstetrics, Including the Pathology 
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MEDICAL BOOKS. 21 



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MEDICAL BOOKS. J8 



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24 SUBJECT CATALOGUE. 

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MEDICAL BOOKS. 25 

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26 SUBJECT3CATAL0QUE. 

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VETERINARY. 

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No. 4. BRUBAKER. PHYSIOLOGY. Eleventh Edition. lUua. 

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No. 19. KYLE. DISEASES OF THE EAR, NOSE, AND 
THROAT. lUuatratcd. 

27 



DA COSTA 



Clinical Hematology 



A Practical Guide to the Examination of the Blood by 
Clinical Methods. With Reference to the Diagnosis of 
Disease. With Colored Illustrations. Cloth, ^5-00 

*^* A new, thorough, systematic, and comprehensive 
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blood, and second, how to diagnose from such examination 
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author's aim has been to cover not alone the field of original 
research, but to supply a book for the student, the hospital 
physician and the general practitioner. It will be found 
wanting in none of these respects. 

OERTEL 



Medical Microscopy 



A GUIDE TO DIAGNOSIS, ELEMEN- 


TARY 


LABORATORY 


METHODS, 


AND 


MICROSCOPIC 


TECHNIC 



By T. E. Oertel, M.D., 

Professor of Pathology and Clinical Microscopy, Medical Depart- 
ment, University of Georgia. 

WITH 131 ILLUSTRATIONS, izmo. Cloth, $*.oa 

28 



The Pocket CyclopediaL of 
Medicine and Surgery 

Full Limp Leather, Round Corners, Gilt Edges, $1.00 
With Thumb Index, $1.25 

Uniform "with ^^ Gould's Pocket Dictionary'^ 



A concise practical volume of nearly 600 
pages, containing a vast amount of infor- 
mation on all medical subjects, including 
Diagnosis and Treatment of Disease, 
witli Formulas and Prescriptions, Emer- 
gencies, Poisons, Drugs and Their Uses, 
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in both English and Metric Systems, etc. 

By Drs. Gould and Pyle 

Based upon their lai^e ** Cyclopedia of 
Medicine and Surgery.** ^ ^ ^ 



*^* This is a new book which will prove of the greatest 
value to students. It is to the broad field of general medi- 
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words. The articles are concise but thorough, and arranged 
in shape for quick reference. In no other book can be 
found so much exact detailed knowledge so conveniently 
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It is Multum in Paruo. Sample Pages Free. 
29 



A NEW EDITION 



Crocker on the Skin 



The Diseases of the Skin. Their Description, Pathology, 
Diagnosis, and Treatment, with Special Reference to the 
Skin Eruptions of Children. By H. Radcliffe Crocker, 
M.D., Physician to the Department of Skin Diseases, Uni- 
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Third Edition, Rewritten and Enlarged 

OCTAVO. JUST READY? CLOTH, $5.00 

*^^ This new edition will easily hold the high position 
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logical Societies, and a recognized authority the world over. 



STURGIS— MANUAL OF 
VENEREAL DISEASES 



By F. R. Sturgis, m.d.. Sometime Clinical Professor of 
Venereal Diseases in the Medical Department of the Uni- 
versity of the City of New York; Seventh Edition, Revised 
and in Part Rewritten by the Author and FOLLEN Cabot, 
M.D., Instructor in Genito-Urinary and Venereal Diseases 
in the Cornell University Medical College. i2mo. 216 
pages. Cloth, j^i.25 

■^^* This manual was originally written for students' 
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the general physician, together with the most approved 
remedies. 



FOR THE DISSECTING ROOM 

Holden*s Anatomy — Seventh Edition 
320 Illustrations 

A Manual of the Dissections of the Human Body. By John 
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Demonstrator of Anatomy, Jefferson Medical College, Phila- 
delphia, etc. 320 Illustrations. Two small compact vol- 
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445 pages. 167 Illustrations. 

Oil Cloth, ^1.50 
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Hughes aLnd Keith — Dissections 
lilustr^Lted 

A Manual of Dissections by Alfred W. Hughes, m.b., 
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Medical Faculty, King's College, London, etc., and Arthur 
Keith, m.d.. Joint Lecturer on Anatomy, London Hospital 
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I. Upper and Lower Extremity. 38 Plates, 116 other 
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11. Abdomen. Thorax. 4 Plates, 149 other Illus- 
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*^ The student will find it of great advantage to have 
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31 



EDGAR'S 

OBSTETRICS 

A NEW TEXT -BOOK 
1 2 2 1 Illustrations 



Edgar's Obstetrics excels all 
other v/orks on this subject 
in completeness, in uni- 
formity and consistency in 
arrangement, thoroughness 
and clearness in handling 
details, and in the number 
and usefulness of its illus- 
trations. 

OCTAVO. CLOTH, $6.00; SHEEP, ^7.00 



JAN 29 190* 



'■^''I¥^ 



